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Abe, Toshiaki; Saigo, Yoko; Hojo, Masayoshi; Kano, Tetsuya; Wakusawa, Ryosuke; Tokita, Yumi; Tamai,Makoto (2006): Protection of photoreceptor cells from phototoxicity by transplanted retinal pigment epithelialcells expressing different neurotrophic factors. In: Cell transplantation, Jg. 14, H. 10, S. 799–808.Abstract Transplantation of cells or tissues and the intravitreal injection of neurotrophic

factors are two methods that have been used to treat retinal diseases. The purposeof this study was to examine the effects of combining both methods: thetransplantation of retinal pigment epithelial (RPE) cells expressing differentneurotrophic factors. The neutrophic factors were Axokine, brain derived-neurotrophic factor (BDNF), and basic fibroblast growth factor (bFGF). Theenhanced green fluorescence protein (eGFP) gene was used as a reporter gene.These genes were transduced into RPE cells by lipofection, selected by antibiotics,and transplanted into the subretinal space of 108 rats. The rats were examined at 1week and 3 months after the transplantation to determine whether the transducedcells were present, were expressing the protein, and were able to protectphotoreceptors against phototoxicity. The survival of the transplanted cells wasmonitored by the presence of eGFP. The degree of protection was determined bythe thickness of the outer nuclear layer. Our results showed that the degree ofphotoreceptor protection was different for the different types of neurotrophic factorsat 1 week. After 3 months, the number of surviving transplanted cell was markedlyreduced, and protection was observed only with the BDNF-transduced RPE cells. Asignificant degree of rescue was also observed by BDNF-transduced RPE cells inthe nontransplanted area of the retina at both the early and late times. Lymphocyticinfiltration was not detected in the vitreous, retina, and choroid at any time. Weconclude that the transplantation of BDNF-transduced RPE cells can reduce thephotoreceptor damage induced by phototoxicity in the transplanted area and weaklyin the nontransplanted area.

Schlagwörter Animals; Brain-Derived Neurotrophic Factorbiosynthesisgeneticsphysiology; CellSurvival; Cell Transplantation; Ciliary NeurotrophicFactorbiosynthesisgeneticsphysiology; Dermatitis,Phototoxicpathologyphysiopathologyprevention & control; Fibroblast Growth Factor2biosynthesisgeneticsphysiology; Gene Expression Regulation; Genes, Reporter;Green Fluorescent Proteinsanalysisgenetics; Lightadverse effects; Nerve GrowthFactorsbiosynthesisgeneticsphysiology; Pigment Epithelium ofEyechemistrycytologymetabolismtransplantation; Rats; Rats, Long-Evans; Rats,Sprague-Dawley; Retinal Rod Photoreceptor Cellscytologyphysiology;Transduction, Genetic

Albrecht-Buehler, G. (1977): Phagokinetic tracks of 3T3 cells: parallels between the orientation of tracksegments and of cellular structures which contain actin or tubulin. In: Cell, Jg. 12, H. 2, S. 333–339.Abstract Phagokinetic tracks were used to determine the current direction of migration in 3T3

cells. Comparing this direction with the orientation of actin or tubulin-containingcellular structures by indirect immunofluorescence, the following results wereobtained. First, the main actin-containing bundles were located at the bottom andtail end of 3T3 cells and ran parallel to the current or preceding direction ofmigration. Second, the 3 micrometer long rod-like structure (primary cilium), whichcontains tubulin and which has been observed by other investigators intransmission electron microscopy (Barnes, 1961; Sorokin, 1962; Wheatley, 1969)and in indirect immunofluorescence (Osborn and Weber, 1976), was orientedpredominantly parallel to the substrate and to the current movement direction. Itseems possible that the primary cilium has a role in the directional control of amigrating 3T3 cell, and that the main actin containing bundles act as substrate-attached rails along which the nucleus and bulk cytoplasm slide duringdisplacement of the cells.

Schlagwörter Actins; Cell Line; Cell Movement; Cilia; Fluorescent Antibody Technique;Glycoproteins; Microtubules; Tubulin

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Albrecht-Buehler, G. (1997): Autofluorescence of live purple bacteria in the near infrared. In: Experimental cellresearch, Jg. 236, H. 1, S. 43–50. Online verfügbar unter doi:10.1006/excr.1996.3688.Abstract We have developed a novel microscope with which to study the fluorescence of

cells in the near-infrared region (lambda = 750-2500 nm). For one of its firstapplications we report on the autofluorescence of live purple bacteria,Rhodospirillum rubrum, and suggest that the autofluorescent component isbacteriochlorophyll. The rapid fading of the autofluorescence of fixed bacteria andof purified bacteriochlorophyll suggests that the live bacteria are able to regeneratetheir pigment with a time constant of approximately 20 s.

Schlagwörter Bacteriochlorophylls; Infrared Rays; Microscopy, Fluorescence; Rhodospirillumrubrum; Time Factors

Allen, Karen Miller (1983): Artificial lighting and health. A selected bibliography. Monticello Ill.: VanceBibliographies (Architecture series--bibliography, A-1087).Schlagwörter Fluorescent lighting; Physiological effect; Bibliography.; Health aspects; Electric

lighting

Amick, Charles L. (1947): Fluorescent lighting manual. 2nd ed. Fluorescent lighting (Hg.). New York: McGraw-Hill.Schlagwörter Fluorescent lighting.

Arai, Takao; Tani, Satoshi; Isoshima, Akira; Nagashima, Hiroyasu; Joki, Tatsuhiro; Takahashi-Fujigasaki, Junko;Abe, Toshiaki (2006): [Intraoperative photodynamic diagnosis for spinal ependymoma using 5-aminolevulinicacid: technical note]. In: No shinkei geka. Neurological surgery, Jg. 34, H. 8, S. 811–817.Abstract OBJECTIVE: The fluorescence-guided resection using 5-aminolevulinic acid (5-

ALA) is a well established method for the treatment of brain tumor, especiallymalignant glioma. However, there is no report on photodynamic diagnosis (PDD) forspinal tumor. In the present study, we evaluated the usefulness of PDD for spinalependymoma using 5-ALA. METHODS: Three patients with spinal ependymomareceived oral doses of 5-ALA (20 mg/kg body weight) 2 hours before anesthesiainduction. Intraoperatively, fluorescence was observed with a 420 nm sharp cut filterafter excitation with a violet semiconductor laser (405 nm) and was verified byanalysis of fluorescent spectra. Residual fluorescent samples taken from the tumorcavity were examined histologically RESULTS: Fluorescence peaked at 636nm inthe removed tumors in all cases. Fluorescent tissue tended to exist at the cranialand caudal portion in the tumor cavity or around the anterior median fissure. Theresidual fluorescent tissue was not detected after removal of the tumor in case 1.The residual fluorescent tissue was composed of tumor cells and ependymal liningin case 2 or the infiltrated inflammatory cells and vascular endothelial cells in case3. Postoperative magnetic resonance (MR) imaging showed no residual tumor inany of the cases. CONCLUSION: The results of this study indicate the usefulnessof 5-ALA-induced tumor fluorescence in guiding resection of spinal ependymoma.5-ALA-induced porphyrin fluorescence may label spinal ependymomas easily andclearly enough to enhance the completeness of tumor removal.

Schlagwörter Adult; Aminolevulinic Acid; Ependymoma; Female; Fluorescence; Humans;Intraoperative Period; Lighting; Magnetic Resonance Imaging; Male; Middle Aged;Photosensitizing Agents; Porphyrins; Sensitivity and Specificity; Spinal CordNeoplasms

Atkinson, Arthur Dinham Stephen (1944): Fluorescent lighting. Dealing with the principles and practice offluorescent lighting, for electrical engineers, illuminating engineers and architects. London: Newnes.Schlagwörter Fluorescent lighting.

Atkinson, Arthur Dinham Stephen (1946): Fluorescent lighting. Brooklyn N.Y.: Chemical publishing co. inc.Schlagwörter Fluorescent lighting.

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Atkinson, Arthur Dinham Stephen (1951): Modern fluorescent lighting. Dealing with the principles and practice offluorescent lighting, for electrical engineers, illuminating engineers, and architects. London: Newnes.Schlagwörter Fluorescent lighting.

Atkinson, Arthur Dinham Stephen (1955): Modern fluorescent lighting. Dealing with the principles and practice offluorescent lighting, for electrical engineers, illuminating engineers, and architects. 2d ed. London: Newnes.Schlagwörter Fluorescent lighting.

Ben-Hur, E.; Elkind, M. M. (1972): Survival response of asynchronous and synchronous Chinese hamster cellsexposed to fluorescent light following 5-bromodeoxyuridine incorporation. In: Mutation research, Jg. 14, H. 2, S.237–245.Schlagwörter Animals; Bromodeoxyuridinemetabolismpharmacology; Cell Line; Cell Survivaldrug

effectsradiation effects; Cells, Culturedradiation effects; Cricetinae;Cysteaminepharmacology; DNAradiation effects; DNA Replication; Fibroblastsdrugeffectsradiation effects; Fluorescence; Light; Mercaptoethylaminespharmacology;Photic Stimulation; Radiation Dosage; Radiation Effects; Radiation-ProtectiveAgents; Radiation-Sensitizing Agents; Time Factors

Ben-Hur, E.; Elkind, M. M. (1972): Damage and repair of DNA in 5-bromodeoxyuridine-labeled Chinese hamstercells exposed to fluorescent light. In: Biophysical journal, Jg. 12, H. 6, S. 636–647. Online verfügbar unterdoi:10.1016/S0006-3495(72)86109-5.Schlagwörter Animals; Bromodeoxyuridinemetabolism; Cell Line; Centrifugation, Density

Gradient; Cricetinae; Cysteaminepharmacology; DNAbiosynthesisradiation effects;DNA Repair; Fibroblastsdrug effectsmetabolismradiation effects; Fluorescence;Isotope Labeling; Kinetics; Light; Molecular Weight; Radiation Effects; Radiation-Protective Agents; Thymidinemetabolism; Tritium

Ben-Hur, E.; Elkind, M. M. (1974): Letter: Damage and repair of DNA in 5-bromodeoxyuridine-labeled Chinesehamster cells exposed to fluorescent light. In: Biophysical journal, Jg. 13, H. 12, S. 1342. Online verfügbar unterdoi:10.1016/S0006-3495(73)86067-9.Schlagwörter Animals; Bromodeoxyuridine; Cell Line; Centrifugation, Density Gradient;

Cricetinae; DNA Repair; DNA, Single-Strandedbiosynthesis; Fluorescence;Molecular Weight

Beral, V.; Evans, S.; Shaw, H.; Milton, G. (1982): Malignant melanoma and exposure to fluorescent lighting atwork. In: Lancet, Jg. 2, H. 8293, S. 290–293.Abstract In a study of 274 women with malignant melanoma, aged 18--54 years, and 549

matched controls in New South Wales, Australia, reported exposure to fluorescentlight at work was associated with a doubling of melanoma risk (relative risk [RR] =2.1; 95% confidence limits 1.32--3.32). The risk grew with increasing duration ofexposure to fluorescent light and was higher in women who had worked mainly inoffices (RR = 2.6) than in women whose main place of work was indoors but not inoffices (RR = 1.8). The findings could not be explained by the differences inhistories of sunlight exposure, in skin or hair colour, or in any other factor. Therewas a relative excess of lesions on the trunk in the group exposed to fluorescentlight at work. 27 men with melanoma and 35 similarly aged controls were studied,and a significant increase in risk was also found: the RB in those exposed forgreater than or equal to 10 years compared with those exposed for less than 10years was 4.4 (95% confidence limits 1.1--17.5). Such an association has not beenreported before, but it is plausible and could explain many of the paradoxicalfeatures of the epidemiology of melanoma. Until more data accumulate it must,however, be viewed cautiously.

Schlagwörter Adolescent; Adult; Age Factors; Female; Fluorescence; Humans; Lightadverseeffects; Lighting; Melanomaetiology; Middle Aged; Occupational Diseasesetiology;Risk; Sex Factors; Skin Neoplasmsetiology

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Boatright, Jeffrey H.; Moring, Anisha G.; McElroy, Clinton; Phillips, Michael J.; Do, Vi T.; Chang, Bo et al. (2007):Tool from ancient pharmacopoeia prevents vision loss. In: Molecular vision, Jg. 12, S. 1706–1714.Abstract PURPOSE: Bear bile has been used in Asia for over 3,000 years to treat visual

disorders, yet its therapeutic potential remains unexplored in Western visionresearch. The purpose of this study was to test whether treatment of miceundergoing retinal degeneration with tauroursodeoxycholic acid (TUDCA), a primaryconstituent of bear bile, alters the course of degeneration. METHODS: Two retinaldegeneration models were tested: the rd10 mouse, which has a point mutation inthe gene encoding the beta subunit of rod phosphodiesterase, and light inducedretinal damage (LIRD). For LIRD studies, albino Balb/C adult mice weresubcutaneously injected with TUDCA (500 mg/kg body weight) or vehicle (0.15 MNaHCO(3)). Sixteen h later, each mouse received repeat injections. Half of eachtreatment group was then placed in bright light (10,000 lux) or dim light (200 lux) forseven h. At the end of exposure, animals were transferred to their regular housing.Electroretinograms (ERGs) were assessed 24 h later, mice sacrificed, eyesembedded in paraffin and sectioned, and retina sections assayed for morphologyand apoptosis by TUNEL and anti-active caspase-3 immunoreactivity viafluorescent confocal microscopy. A subset of mice were sacrificed 8 and 15 daysafter exposure and retina sections analyzed for morphology and apoptosis. For rd10studies, mice were injected subcutaneously with TUDCA or vehicle at postnatal (P)days 6, 9, 12, and 15. At p18, ERGs were recorded, mice were euthanized andeyes were harvested, fixed, and processed. Retinal sections were stained (toluidineblue), and retinal cell layers morphometrically analyzed by light microscopy.Consecutive sections were analyzed for apopotosis as above. RESULTS: By everymeasure, TUDCA greatly slowed retinal degeneration in LIRD and rd10 mice. ERGa-wave and b-wave amplitudes were greater in mice treated with TUDCA comparedto those treated with vehicle. Retinas of TUDCA-treated mice had thicker outernuclear layers, more photoreceptor cells, and more fully-developed photoreceptorouter segments. Finally, TUDCA treatments dramatically suppressed signs ofapoptosis in both models. CONCLUSIONS: Systemic injection of TUDCA, a primaryconstituent of bear bile, profoundly suppressed apoptosis and preserved functionand morphology of photoreceptor cells in two disparate mouse models of retinaldegeneration. It may be that bear bile has endured so long in Asian pharmacopeiasdue to efficacy resulting from this anti-apoptotic and neuroprotective activity ofTUDCA. These results also indicate that a systematic, clinical assessment ofTUDCA may be warranted.

Schlagwörter Animals; Apoptosisdrug effects; Bilechemistry; Blindnessetiologyprevention &control; Cyclic Nucleotide Phosphodiesterases, Type 6; Disease Models, Animal;Electroretinography; Injections, Subcutaneous; Light; Medicine, East AsianTraditional; Mice; Mice, Mutant Strains; Phosphoric Diester Hydrolasesgenetics;Photoreceptor Cells, Vertebratedrug effectspathology; RetinalDegenerationcomplicationsetiologygeneticsphysiopathology;Taurochenodeoxycholic Acidadministration & dosagechemicalsynthesispharmacology; Ursidae

Brondon, Philip; Stadler, Istvan; Lanzafame, Raymond J. (2005): A study of the effects of phototherapy doseinterval on photobiomodulation of cell cultures. In: Lasers in surgery and medicine, Jg. 36, H. 5, S. 409–413.Online verfügbar unter doi:10.1002/lsm.20183.Abstract BACKGROUND AND OBJECTIVES: Dosimetry and treatment frequency are

controversial phototherapy issues. Efficacy of dose fractionation onphotobiomodulation was evaluated in vitro. STUDY DESIGN/MATERIALS ANDMETHODS: Human HEP-2 and murine L-929 cell lines were cultured in completeDMEM media. Photoradiation (670 nm, 5 J/cm2/treatment, 50 J/cm2 total energydelivery), was performed varying treatments per 24 hour period: Group I (Controls)-0, Group II-1/d, Group III-2/d, Group IV-4/d. Cell proliferation was measured using

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - CitaviCyquant (fluorescent DNA content) and MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrasolium bromide) assays for 240 hours post therapy. A proliferationindex: PI = (#Cells Experimental(t) / #Cells Control(t)) was computed. RESULTS:MTT assay results demonstrated maximal response in Group III (P < 0.05, n = 3).Cyquant maxima occurred in HEP-2 Groups II and III (P < 0.045) and L-929 GroupIII (P < 0.091). CONCLUSIONS: Cellular response to dose frequency varies. Morefrequent treatments (2/24 hours) increased metabolism and proliferation in both celllines. Further investigation of dose fractionation in phototherapy is warranted.

Schlagwörter Animals; Cell Line; Cell Proliferation; Coloring Agents; Connective Tissue Cells;Dose Fractionation; Epithelial Cells; Humans; Mice; Phototherapy; TetrazoliumSalts; Thiazoles; Time Factors

Bulina, Maria E.; Lukyanov, Konstantin A.; Britanova, Olga V.; Onichtchouk, Daria; Lukyanov, Sergey;Chudakov, Dmitriy M. (2006): Chromophore-assisted light inactivation (CALI) using the phototoxic fluorescentprotein KillerRed. In: Nature protocols, Jg. 1, H. 2, S. 947–953. Online verfügbar unterdoi:10.1038/nprot.2006.89.Abstract The phototoxic red fluorescent GFP-like protein KillerRed has recently been

described. The phototoxicity of KillerRed exceeds that of EGFP by at least 1,000-fold, making it the first fully genetically encoded photosensitizer. KillerRed opens upnew possibilities for precise light-induced cell killing and target protein inactivation.Because KillerRed is encoded by a gene, it can be expressed in a spatially andtemporally regulated manner, under a chosen promoter, and fused with the desiredprotein of interest or localization signal. Here we provide a protocol for target proteininactivation in cell culture using KillerRed. As KillerRed is a new tool, the protocolfocuses on aspects that will allow users to maximize the potential of this protein,guiding the design of chimeric constructs, recommended control experiments andpreferred illumination parameters. The protocol, which describes target proteinvisualization and subsequent inactivation, is a 2- or 3-d procedure.

Schlagwörter Bacteria; Epithelial Cells; Gene Expression Regulation; Green Fluorescent Proteins;Hela Cells; Humans; Light; Luminescent Agents; Protein Binding

Chaloupka, R.; Sureau, F.; Kocisova, E.; Petrich, J. W. (1998): Hypocrellin A photosensitization involves anintracellular pH decrease in 3T3 cells. In: Photochemistry and photobiology, Jg. 68, H. 1, S. 44–50.Abstract The fluorescent pH probe carboxy-seminaphtorhodafluor-1 (C-Snarf-1) has been

used for laser microspectro-fluorometric assays of intracellular pH in 3T3 mousefibroblasts treated with hypocrellin A. These results are compared to thosepreviously obtained with the structurally related hydroxylated polycyclic quinone,hypericin (Sureau et al., J. Am. Chem. Soc. 118, 9484-9487, 1996). A mean localintracellular pH drop of 0.6 units has been observed in the presence of 1 microMhypocrellin A after 90 s of exposure to 0.1 microW of laser irradiation at 514.5 nm.The time evolution of the cytoplasm acidification for hypocrellin A-treated cells isfaster than that for cells treated by hypericin. Thus, release of protons from anexcited state of hypocrellin A appears to be more efficient than that from hypericin.In addition, the pH dependence of the quenching of C-Snarf-1 fluorescence in 3T3cells under continuous irradiation has been observed. It is shown here that undercontinuous illumination, a pH decrease is able to induce a modification of theintracellular binding equilibrium of C-Snarf-1 that results in an increase of C-Snarf-1fluorescence intensity. This latter observation suggests that the protons generatedupon the photoexcitation of hypericin or its analogs may be involved in theproduction of other photoreactive species. Finally, we suggest that, just as forhypericin, this pH drop may be involved in the antiviral and antitumor activity ofhypocrellin A.

Schlagwörter 3T3 Cells; Animals; Benzopyrans; Fluorescent Dyes; Hydrogen-Ion Concentration;Intracellular Fluid; Lasers; Mice; Naphthols; Perylene; Photobiology;Photosensitizing Agents; Quinones; Rhodamines

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - CitaviDuncan, T. E.; O'Steen, W. K. (1986): The diurnal susceptibility of rat retinal photoreceptors to light-induceddamage. In: Experimental eye research, Jg. 41, H. 4, S. 497–507.Abstract Exposure of albino rats to high intensity light results in rapid, graded loss of

photoreceptors. The hormonal status and age of an animal at the time of exposureaffect the severity of light-induced retinal damage. The adrenal axis and pituitaryhormones (prolactin) have been demonstrated previously to affect the degree of celldeath in the retina. Because circadian rhythms for adrenal and pituitary secretionhave been demonstrated in the rat, a series of experiments was undertaken todetermine if a diurnal pattern of retinal susceptibility to light damage exists whichmight be related to endogenous endocrine rhythms. Male Sprague-Dawley ratswere exposed to 4 hr of high intensity fluorescent light for 8 consecutive days duringdifferent phases of the 14:10 hr light: dark animal room light cycle. Morphometricanalysis performed at the light microscopic level 2 weeks after exposuredemonstrated a differential susceptibility to light-induced cell death depending uponthe period during the light-dark cycle when animals received their daily lightexposure. Neuronal cell death was confined to the outer nuclear layer as previouslydescribed. The retinas of animals exposed during the middle of the dark period orduring the first 5 hr of the light period were significantly more damaged than theretinas of animals exposed during the last 9 hr of the light period. Control groups forthe relative amounts of dark-adaptation between groups suggested that the diurnalsusceptibility to light damage was not solely dependent upon the degree of darkadaptation. These results demonstrate a diurnal susceptibility of photoreceptors tolight-induced cell death.

Schlagwörter Animals; Cell Survivalradiation effects; Circadian Rhythm; Dark Adaptation; Light;Male; Photometry; Photoreceptor Cellsradiation effects; Rats; Rats, Inbred Strains;Time Factors

Elenbaas, W. (1959): Fluorescent lamps and lighting. New York: Macmillan (Phillips' technical library).Schlagwörter Fluorescent lighting.; Fluorescent lamps.

Elenbaas, W. (1971): Fluorescent lamps. 2nd ed. London: Macmillan (Philips technical library).Schlagwörter Fluorescent lighting.; Fluorescent lamps.

Federal Construction Council; Task Group T-58 (1968): High-frequency lighting. United States. (Hg.).Washington: National Academy of Sciences (National Academy of Sciences. Publication 1610., no. 53).Schlagwörter Fluorescent lighting.

Forsythe, William Elmer; Adams, Elliot Quincy (1948): Fluorescent and other gaseous discharge lamps. NewYork: Technical Division Murray Hill Books.Schlagwörter Fluorescent lighting.; Electric discharge lighting.

Gaillard, E. R.; Atherton, S. J.; Eldred, G.; Dillon, J. (1995): Photophysical studies on human retinal lipofuscin.In: Photochemistry and photobiology, Jg. 61, H. 5, S. 448–453.Abstract Fluorescent material generated in the human retina accumulates within lipofuscin

granules of the retinal pigment epithelium (RPE) during aging. Its presence hasbeen suggested to contributed to various diseases including age-related maculardegeneration. Because this material absorbs light at wave lengths as long as 550nm, photophysical studies were performed to determine whether lipofuscin couldcontribute to light damage and to determine if its composition is similar to asynthetically prepared lipofuscin. Time-resolved experiments were performed tomonitor (1) fluorescence decay, (2) the UV-visible absorption of longer-lived excitedstates and (3) the formation and decay of singlet oxygen at 1270 nm. Steady-stateand time-resolved fluorescence studies indicate that human and synthetic lipofuscinhave fluorophores in common. Time-resolved absorption experiments on humanretinal lipofuscin and synthetic lipofuscin showed the presence of at least twotransient species, one absorbing at 430 nm (lifetime ca 7 microseconds) and a

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavisecond absorbing at 580 nm, which decays via second order kinetics. In addition,there is a third absorbing species stable to several hundred milliseconds. Thetransient species at 430 nm is quenched by oxygen, suggesting that it is a tripletstate. Subsequent studies showed the formation of singlet oxygen, which wasmonitored by its phosphorescence decay at 1270 nm. These studies demonstratethat lipofuscin can act as a sensitizer for the generation of reactive oxygen speciesthat may contribute to the age-related decline of RPE function and blue lightdamage.

Schlagwörter Adult; Humans; Kinetics; Lipofuscinchemistryisolation & purification;Photochemistry; Photolysis; Pigment Epithelium of Eyemetabolism; ProteinConformation; Quantum Theory; Spectrometry, Fluorescence; Spectrophotometry

Gantt, R.; Parshad, R.; Ewig, R. A.; Sanford, K. K.; Jones, G. M.; Tarone, R. E.; Kohn, K. W. (1978): Fluorescentlight-induced DNA crosslinkage and chromatid breaks in mouse cells in culture. In: Proceedings of the NationalAcademy of Sciences of the United States of America, Jg. 75, H. 8, S. 3809–3812.Abstract A single 20-hr exposure of mouse cells derived from embryonic or lung tissue to

cool-white fluorescent light (4.6 W/m2) causes both DNA damage and chromosomeaberrations including chromatid breaks, exchanges, and minutes. In Kohn's alkalineelution technique, the DNA from exposed cells elutes more slowly than that fromshielded cells. Because larger molecular weight DNA elutes slower than smaller, weinterpret these results to mean that the DNA in cells exposed to light is crosslinked.The estimated frequency of crosslinks is sufficient to account for the number ofchromatid breaks observed. The types of chromosome aberrations produced bylight indicate that the primary lesion results in chromatid rather than chromosomebreaks, and the results suggest an influence of cell density in that cells in denselypopulated cultures showed few or no chromatid breaks after irradiation. The presentresults, together with observations from the literature, suggest that the DNAcrosslinkage and the chromosome aberrations produced by light may be related.

Schlagwörter Cells, Cultured; Chromatidsradiation effects; Chromosome Aberrations;DNAradiation effects; Fluorescence; Lightadverse effects; Time Factors

Gordon, William C.; Casey, Douglas M.; Lukiw, Walter J.; Bazan, Nicolas G. (2002): DNA damage and repair inlight-induced photoreceptor degeneration. In: Investigative ophthalmology & visual science, Jg. 43, H. 11, S.3511–3521.Abstract PURPOSE: Intense light causes photoreceptor death that is greatest in the superior

central retina. Short-duration treatment in a light-damage model results in TUNEL-positive photoreceptor nuclei within this region. However, cells lost 10 days afterlight treatment are fewer than the TUNEL-labeled cells observed earlier. Therefore,this study was undertaken to monitor DNA fragmentation and cell death to explainthe discrepancy. METHODS: Eyes of dark-adapted rats were light damaged for 4 or5 hours. DNA fragmentation was measured by TUNEL, laddering, and highlyrepetitive short interspersed nuclear element (SINE) analysis in dark-adapted,nondamaged control (dark-control) retinas and in retinas collected at 6-hourintervals after light treatment. TUNEL-positive photoreceptor nuclei were counted inthese samples along a superior-to-inferior meridian and compared with control anddamaged 10-day retinas. Monocytes and DNA polymerase beta were monitored byimmunohistochemistry. RESULTS: TUNEL-positive staining of photoreceptors wascentered around the superior central retina. At 10 days, photoreceptor loss hadoccurred in this region. In graphs of 6-hour-interval data, two DNA-fragmentationpeaks, 24 hours apart, were evident. Monocytes appeared after nuclear damage.Total TUNEL-positive cells under both peaks exceeded the number ofphotoreceptors lost. The DNA-repair enzyme, polymerase beta, was induced in thesuperior central retina, within photoreceptor inner segments, 24 hours after lighttreatment, but declined thereafter. CONCLUSIONS: One population of damagedcells may mend DNA until the repair mechanism is exceeded and then revert toapoptosis, or, alternatively, two populations may undergo DNA fragmentation 24

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavihours apart. Either DNA fragmentation is masked at midpoint by temporary repair,or two waves of damage occur, but repair rescues the first set, not the second.Photoreceptors lost are fewer than TUNEL-positive cells. Thus, both possibilitiessuggest photoreceptor DNA repair. The transient appearance of DNA polymerasebeta in photoreceptors under these experimental conditions further suggestsnuclear repair. Thus, maintenance of in-house DNA-repair mechanisms mayprovide an alternate approach for the rescue of photoreceptors, as well as otherneurons with stress-induced damage. These events may provide useful drugtargets to promote photoreceptor survival in various forms of retinal degeneration.

Schlagwörter Animals; Blotting, Western; DNAanalysis; DNA Damageradiation effects; DNAFragmentation; DNA Polymerase betametabolism; DNA Repair; FluorescentAntibody Technique, Indirect; In Situ Nick-End Labeling; Light; Male; PhotoreceptorCells, Vertebratepathologyradiation effects; Proliferating Cell NuclearAntigenmetabolism; Radiation Injuries, Experimentalgeneticsmetabolismpathology;Rats; Rats, Sprague-Dawley; Retinal Degenerationgeneticsmetabolismpathology;Time Factors; Up-Regulation

Heeke, D. S.; White, M. P.; Mele, G. D.; Hanifin, J. P.; Brainard, G. C.; Rollag, M. D. et al. (1999): Light-emittingdiodes and cool white fluorescent light similarly suppress pineal gland melatonin and maintain retinal functionand morphology in the rat. In: Laboratory animal science, Jg. 49, H. 3, S. 297–304.Abstract BACKGROUND AND PURPOSE: A novel light-emitting diode (LED) light source for

use in animal-habitat lighting was evaluated. METHODS: The LED was evaluatedby comparing its effectiveness with that of cool white fluorescent light (CWF) insuppressing pineal gland melatonin content and maintaining normal retinalphysiology, as evaluated by use of electroretinography (ERG), and morphology.RESULTS: Pineal melatonin concentration was equally suppressed by LED andCWF light at five light illuminances (100, 40, 10, 1, and 0.1 lux). There were nosignificant differences in melatonin suppression between LED and CWF light,compared with values for unexposed controls. There were no differences in ERG a-wave implicit times and amplitudes or b-wave implicit times and amplitudesbetween 100-lux LED-exposed rats and 100-lux CWF-exposed rats. Results ofretinal histologic examination indicated no differences in retinal thickness, rod outersegment length, and number of rod nuclei between rats exposed to 100-lux LEDand 100-lux CWF for 14 days. Furthermore, in all eyes, the retinal pigmentedepithelium was intact and not vacuolated, whereas rod outer segments were ofnormal thickness. CONCLUSION: LED light does not cause retinal damage and cansuppress pineal melatonin content at intensities similar to CWF light intensities.

Schlagwörter Animals; Electroretinographyradiation effects; Lightadverse effects; Male;Melatoninmetabolism; Pineal Glandmetabolismradiation effects;Radioimmunoassay; Rats; Rats, Sprague-Dawley; Retinaphysiologyradiationeffects

Kasperowski, Walther (195?): Mehr Licht durch Leuchtstofflampen. Technik und Anwendung derFluoreszenzbeleuchtung. Wien: A. Göschl.Schlagwörter Fluorescent lighting.

Katz, M. L.; Eldred, G. E. (1989): Retinal light damage reduces autofluorescent pigment deposition in the retinalpigment epithelium. In: Investigative ophthalmology & visual science, Jg. 30, H. 1, S. 37–43.Abstract Lipofuscin in the retinal pigment epithelium (RPE) is thought to be derived from

phagocytosed photoreceptor outer segment disc membranes. Based on thishypothesis, one would predict that the rate of lipofuscin deposition in the RPE wouldbe proportional to the density of photoreceptor cells in the retina. In previous studiesit was demonstrated that specific loss of photoreceptor cells due to a genetic defectresulted in a substantial decrease in the rate of age-related lipofuscin accumulationin the RPE. In order to confirm that this decreased RPE lipofuscin deposition wasdirectly related to reduced photoreceptor cell density, experiments were conducted

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavito determine whether light-induced photoreceptor cell destruction affected RPElipofuscin content. The effects of retinal light damage on RPE autofluorescentpigment accumulation resulting from both normal aging and vitamin E deficiencywere examined. Starting immediately after weaning, albino Fisher 344 rats were feddiets either containing or lacking vitamin E. All animals were maintained on a 12hr/12 hr light/dark cycle. During the light phases of the cycles, the cage illuminancefor one-half the animals in each dietary group was 750 lux, while the remaining ratswere exposed to a light level of 15 lux. Illumination was provided by 40 watt cool-white fluorescent lamps. After 17 weeks, rats in both dietary groups that weremaintained under the higher light intensity had substantially reduced photoreceptorcell densities relative to animals in the same dietary group maintained under dimlight conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Schlagwörter Agingmetabolism; Animals; Chromatography, Thin Layer; Fluorescence;Lightadverse effects; Lipofuscinmetabolism; Male; Pigment Epithelium ofEyemetabolism; Rats; Rats, Inbred F344; Retinainjuries; RetinalPigmentsmetabolism; Vitamin E Deficiencymetabolism

Kehat, Rinat; Zemel, Esther; Cuenca, Nicolas; Evron, Tama; Toiber, Debra; Loewenstein, Anat et al. (2007): Anovel isoform of acetylcholinesterase exacerbates photoreceptors death after photic stress. In: Investigativeophthalmology & visual science, Jg. 48, H. 3, S. 1290–1297. Online verfügbar unter doi:10.1167/iovs.06-0847.Abstract PURPOSE: To study the involvement of stress-induced acetylcholinesterase

(AChE) expression in light-induced retinal damage in albino rats. METHODS: Adultalbino rats were exposed for 24 hours to bright, damaging light. AChE expressionwas monitored by in situ hybridization, by histochemistry for AChE activity, and byimmunocytochemistry. An orphan antisense agent (Monarsen; EsterNeurosciences, Ltd., Herzlia Pituach, Israel) was administered intraperitoneally tominimize light-induced AChE expression. The electroretinogram (ERG) wasrecorded to assess retinal function. RESULTS: Twenty-four-hour exposure to brightlight caused severe reduction in the ERG responses and augmented expression ofmRNA for the "read-through" variant of AChE (AChE-R) in photoreceptor innersegments (IS), bipolar cells, and ganglion cells. AChE activity increased in IS. Theexpressed AChE protein was a novel variant, characterized by an extended Nterminus (N-AChE). Systemic administration of the orphan antisense agent,Monarsen, reduced the photic induction of mRNA for AChE-R, and of the N-AChEprotein. Rats exposed to bright, damaging light and treated daily with Monarsenexhibited larger ERG responses, relatively thicker outer nuclear layer (ONL), andmore ONL nuclei than did rats exposed to the same damaging light but treated dailywith saline. CONCLUSIONS: The findings indicate that the photic-induced novelvariant of AChE (N-AChE-R) may be causally involved with retinal light damage andsuggest the use of RNA targeting for limiting such damage.

Schlagwörter Acetylcholinesterasegeneticsmetabolism; Animals; Cell Death; DNA,Antisensepharmacology; Electroretinographyradiation effects; Fluorescent AntibodyTechnique, Indirect; Gene Expression Regulation, Enzymologicphysiology; In SituHybridization; Isoenzymesmetabolism; Light; Male; Microscopy, Confocal;Photoreceptor Cells, Vertebratepathology; RNA, Messengermetabolism; RadiationInjuries, Experimentalenzymology; Rats; Rats, Sprague-Dawley; Retinaradiationeffects; Retinal Degenerationenzymologypathology

Kennedy, A. R.; Ritter, M. A.; Little, J. B. (1980): Fluorescent light induces malignant transformation in mouseembryo cell cultures. In: Science (New York, N.Y.), Jg. 207, H. 4436, S. 1209–1211.Abstract Fluorescent light induced a dose-dependent malignant transformation in mouse

C3H10T1/2 cells. A plateau in the dose-response curve for transformation wascorrelated with that observed with ultraviolet light exposure. The similarity in the twodose-response patterns suggests that similar molecular processes may be involvedin the induction of malignant transformation by the two types of radiation.

Schlagwörter Animals; Cell Survivalradiation effects; Cell Transformation, Neoplasticradiation

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavieffects; Cells, Cultured; DNAradiation effects; Dose-Response Relationship,Radiation; Embryo, Mammalianradiation effects; Fluorescence; Light; Mice;Pyrimidine Dimersradiation effects; Ultraviolet Rays

Koide, R.; Ueda, T. N.; Dawson, W. W.; Hope, G. M.; Ellis, A.; Somuelson, D. et al. (2001): [Retinal hazard fromblue light emitting diode]. In: Nippon Ganka Gakkai zasshi, Jg. 105, H. 10, S. 687–695.Abstract PURPOSE: To compare the effect of exposure time from a blue(460 nm) light

emitting diode(LED) on the morphology of the outer retina and determine conditionswhere damage occurs. MATERIALS AND METHODS: Young adult rhesusmonkeys were anesthetized, and received blue LED exposure from a modified slit-lamp. A 3 mm beam of 0.85 mW was imaged onto the retina through a lenspositioned before the cornea and exposure damage was determined at timeintervals for 12 to 90 min. Fundus photography, fluorescein angiography(FAG),retinal tomography(HRT), and s-cone electororetinogram(S-ERG) were recorded atbaseline, 2, and 30 days. RESULTS: Two days after 40 min exposure, there was agrey, discolored region, which was over-fluorescent in FAG, and an incresse in HRTand S-ERG corresponding to the site which was exposed to LED light. Inhistological examination at 30 days, the LED had caused produced a markeddisruption of the disks of photoreceptor cells, damaged retinal pigmentepithelium(RPE) apical villi, and a loss of RPE melanin after 90 min exposure.CONCLUSION: A threshold level was found around 40 min. This morphologicaldamage may impair function and continuous exposure to blue light is potentiallydangerous to vision.

Schlagwörter Animals; Lightadverse effects; Macaca mulatta; Male; Pigment Epithelium ofEyeradiation effectsultrastructure; Radiation Injuries, Experimentalpathology;Retinapathologyradiation effects

Laabich, Aicha; Vissvesvaran, Ganesh P.; Lieu, Kuo L.; Murata, Kyoko; McGinn, Tim E.; Manmoto, Corinne C.et al. (2006): Protective effect of crocin against blue light- and white light-mediated photoreceptor cell death inbovine and primate retinal primary cell culture. In: Investigative ophthalmology & visual science, Jg. 47, H. 7, S.3156–3163. Online verfügbar unter doi:10.1167/iovs.05-1621.Abstract PURPOSE: The present study was performed to investigate the effect of crocin on

blue light- and white light-induced rod and cone death in primary retinal cellcultures. METHODS: Primary retinal cell cultures were prepared from primate andbovine retinas. Fifteen-day-old cultures were exposed to blue actinic light or to whitefluorescent light for 24 hours. Cultures were treated by the addition of differentconcentrations of crocin for 24 hours before light exposure or for 8 hours after lightexposure. Cultures kept in the dark were used as controls. Green nucleic acid stainassay was used to evaluate cell death. Rods and cones were immunolabeled withspecific antibodies and counted. TUNEL labeling was used to detect fragmentedDNA in fixed cells after light exposure. RESULTS: Primary retinal cell culturescontained a mixture of retinal cells enriched in photoreceptors, bipolar cells, andMüller cells. Twenty-four-hour exposure to blue and white light induced death in70% to 80% of the photoreceptors in bovine and primate retinal cell cultures. Crocinprotected the photoreceptors against blue light- or white light-mediated damage in aconcentration-dependent manner with an EC50 of approximately 30 microM.TUNEL assays confirmed that crocin protected photoreceptors from light damage.CONCLUSIONS: These results show that blue and white light selectively induce rodand cone cell death in an in vitro model. Crocin protects retinal photoreceptorsagainst light-induced cell death.

Schlagwörter Animals; Carotenoidspharmacology; Cattle; Cell Count; Cell Culture Techniques;Cell Deathdrug effectsradiation effects; Crocus; Dose-Response Relationship,Drug; Flowers; Fluorescent Antibody Technique, Indirect; In Situ Nick-End Labeling;Lightadverse effects; Macaca fascicularis; Photoreceptor Cells, Vertebratedrugeffectsradiation effects; Plant Extractspharmacology; Radiation Injuries,Experimentaletiologyprevention & control; Retinal Degenerationetiologyprevention

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavi& control

Lam, R. W.; Buchanan, A.; Clark, C. M.; Remick, R. A. (1991): Ultraviolet versus non-ultraviolet light therapy forseasonal affective disorder. In: The Journal of clinical psychiatry, Jg. 52, H. 5, S. 213–216.Abstract Although light therapy has been shown to be effective in the treatment of seasonal

affective disorder (SAD), little research has been done to determine which lightwavelengths affect treatment outcome. In this triple crossover study the authorscompared 1 week of light therapy in which bright (2500 lux), full-spectrumfluorescent light, with and without blockade of the ultraviolet (UV) spectrum, wasused with a dim (500 lux) light control in 11 SAD patients. The dim light conditionhad no significant antidepressant effects as measured by the Hamilton Rating Scalefor Depression (HAM-D), the Beck Depression Inventory (BDI), and an atypicaldepressive symptom (ATYP) score. The UV-light condition significantly reducedHAM-D, BDI, and ATYP scores, whereas the UV-blocked condition significantlyreduced only the ATYP score. These results suggest that the UV-spectrum in lighttherapy may have a differential effect on typical and atypical symptoms in SAD.

Schlagwörter Depressive Disorderpsychologytherapy; Evaluation Studies as Topic; Female;Humans; Light; Male; Personality Inventory; Phototherapymethods; PsychiatricStatus Rating Scales; Research Design; Seasons; Ultraviolet Rays; UltravioletTherapy

Lee, F. L.; Yu, D. Y.; Tso, M. O. (1990): Effect of continuous versus multiple intermittent light exposures on ratretina. In: Current eye research, Jg. 9, H. 1, S. 11–21.Abstract The damaging effects of continuous light exposure to the albino rat retina have

been well documented. However, the cumulative effects of multiple light exposuresare not well defined. We therefore compared the retinal injury induced by a single24 hour light exposure with that caused by three intermittent exposures of 8 hourseach. Eight dark-adapted albino Lewis rats were exposed for 24 hours to greenfluorescent light (490-580 nm) at an illuminance level of 175 foot-candles. A secondgroup of 8 rats was exposed under similar conditions in three split doses of 8 hourseach at intervals of 7 days between each exposure. Recovery was allowed in totaldarkness, and the animals were sacrificed 2 weeks following the last exposure.Retinal damage was assessed by morphometry and light and electron microscopy.Mild cumulative retinal injury, mostly in photoreceptor cells with relative sparing ofthe retinal pigment epithelium, was seen in the split dose group, while extensivedamage involving photoreceptor cells and retinal pigment epithelium was noted inthe group exposed continuously for 24 hours.

Schlagwörter Animals; Lightadverse effects; Male; Periodicity; Photoreceptor Cellsradiationeffectsultrastructure; Pigment Epithelium of Eyeradiation effectsultrastructure; Rats;Rats, Inbred Lew; Retinaradiation effectsultrastructure

McColl, S. L.; Veitch, J. A. (2001): Full-spectrum fluorescent lighting: a review of its effects on physiology andhealth. In: Psychological medicine, Jg. 31, H. 6, S. 949–964.Abstract BACKGROUND: Full-spectrum fluorescent lighting (FSFL) has been credited with

causing dramatic beneficial effects on a wide variety of behaviours, mental healthoutcomes and physical health effects, as compared to other fluorescent lamp types.These effects are hypothesized to occur because of similarity between FSFLemissions and daylight, which is said to have evolutionary superiority over otherlight sources. METHOD: This review, covering the period 1941-1999, criticallyconsiders the evidence for direct effects of FSFL through skin absorption as well asindirect effects on hormonal and neural processes. CONCLUSIONS: Overall, theevidence does not show dramatic effects of fluorescent lamp type on behaviour orhealth, neither does it support the evolutionary hypothesis.

Schlagwörter Arousalphysiology; Brainphysiology; Calciummetabolism; Evolution; Female;Fluorescence; Health Status; Humans; Hydrocortisoneurine;Hyperbilirubinemiatherapy; Light; Male; Melatoninurine; Phototherapy; Psychomotor

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - CitaviPerformancephysiology; Seasonal Affective Disordertherapy; Skinradiation effects;Stress, Psychologicalmetabolism; Sympathetic Nervous Systemphysiology; VitaminDmetabolism

Miller, Henry Arthur (1947): Luminous tube lighting. Including high voltage fluorescent lighting. 2d ed. London:Newnes.Schlagwörter Electric discharge lighting.

Miller, Henry Arthur (1949): Cold cathode fluorescent lighting. London: Technical Press.Schlagwörter Fluorescent lighting.

Nell, Walter (1952): Beleuchtungstechnik mit Leuchtstofflampen und Leuchtröhren. Leipzig: Fachbuchverlag.Schlagwörter Fluorescent lighting.

Noell, W. K.; Albrecht, R. (1971): Irreversible effects on visible light on the retina: role of vitamin A. In: Science(New York, N.Y.), Jg. 172, H. 978, S. 76–79.Abstract Diffuse retinal irradiation by visible light produces in the rat the death of visual cells

and pigment epithelium. Typically, cage illumination of 1500 lux from fluorescentlight through a green filter leads to severe damage when continued for 40 hours.Vitamin A deficiency protects against this damage but experiments show that retinolreleased by light from rhodopsin is probably not the toxic agent. Protection againstlight damage depends on a long-range state of cell adaptation to light itself. Thenormal diurnal cycle of light and dark seems to be the essential factor in controllingvisual cell viability and susceptibility.

Schlagwörter Animals; Electrocardiography; Eye Diseasesetiology; Lightadverse effects; Rats;Retina; Retinal Pigmentsmetabolism; Time Factors; VitaminAmetabolismphysiology; Vitamin A Deficiencymetabolism

Okuno, Tsutomu; Saito, Hiroyuki; Ojima, Jun (2002): Evaluation of blue-light hazards from various light sources.In: Developments in ophthalmology, Jg. 35, S. 104–112.Abstract Visible light of short wavelength (blue light) may cause a photochemical injury to the

retina, called photoretinitis or blue-light hazard. In this study, various light sourceswere evaluated for blue-light hazard. These sources include the sun, the arcassociated with arc welding and plasma cutting, molten steel, iron and glass, theinterior of furnaces, the arc or envelope of discharge lamps, the filament orenvelope of incandescent lamps, the envelope of fluorescent lamps and light-emitting diodes. The spectral radiance of each light source was measured, andblue-light effective radiance and the corresponding permissible exposure time perday were calculated in accordance with the ACGIH (American Conference ofGovernmental Industrial Hygienists) standard. The sun, arc welding, plasma cuttingand the arc of discharge lamps were found to have extremely high effectiveradiances with corresponding permissible exposure times of only 0.6-40 s,suggesting that viewing these light sources is very hazardous to the retina. Otherlight sources were found to have low effective radiances under the study conditionsand would pose no hazard, at least for short exposure times.

Schlagwörter Dose-Response Relationship, Radiation; Humans; Light; Maximum AllowableConcentration; Radiation Injuries; Radiation Monitoring; Radiometry; Retina;Retinitis

Paddock, S. W.; Albrecht-Buehler, G. (1988): Rigidity of the nucleus during nuclear rotation in 3T3 cells. In:Experimental cell research, Jg. 175, H. 2, S. 409–413.Abstract Using near infrared microscopy and ultraviolet fluorescence microscopy of living

3T3 cells stained with the fluorochrome Hoechst 33342, we have demonstrated thatthe nucleoli and Hoechst 33342-stained chromocenters in the nucleus maintain afixed pattern during nuclear rotation. We conclude that the term "nuclear rotation"refers to rotation of the entire nucleus in the cytoplasm of interphase cells, and that

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavinuclear rotation is not an expression of karyoplasmic streaming. In conjunction withearlier results on nuclear rotation the data imply that the interface of nuclear rotationis located either between the two nuclear membranes or in the adjacent cytoplasm.

Schlagwörter Benzimidazoles; Cell Nucleus; Fluorescent Dyes; Interphase; Microscopy,Fluorescence; Microscopy, Ultraviolet; Rotation; Video Recording

Parshad, R.; Sanford, K. K.; Jones, G. M. (1985): Chromatid damage induced by fluorescent light during G2phase in normal and Gardner syndrome fibroblasts. Interpretation in terms of deficient DNA repair. In: Mutationresearch, Jg. 151, H. 1, S. 57–63.Abstract Skin fibroblasts from Gardner syndrome (GS) compared with those from normal

donors showed a significantly higher incidence of chromatid gaps and breaksfollowing exposure to low-intensity, cool-white fluorescent light during G2 phase ofthe cell cycle. Considerable evidence supports the concept that chromatid gaps andbreaks seen directly after exposure to DNA-damaging agents represent unrepairedDNA single- and double-strand breaks respectively. The changes in incidence ofchromatid aberrations with time after light exposure are consistent with thesequence of events known to follow DNA damage and repair. Initially, the incidenceof light-induced chromatid gaps was equivalent in GS and normal fibroblasts. In thenormal cells, the chromatid gaps disappeared by 1 h post-exposure, presumably asa result of efficient repair of DNA single-strand breaks. In contrast, the incidence ofgaps increased in GS cells by 0.5 h followed by a decrease at 1 h and concomitantincrease in chromatid breaks. It appears from these findings that the increasedincidence of chromatid damage in GS fibroblasts results from deficient repair ofDNA single-strand breaks which arise from incomplete nucleotide excision of DNAdamage during G2 phase.

Schlagwörter Cells, Cultured; Chromatidsradiation effects; DNA Repair; Dose-ResponseRelationship, Radiation; Gardner Syndromegenetics; Humans; Interphase; Light

Parshad, R.; Sanford, K. K.; Jones, G. M.; Tarone, R. E. (1978): Fluorescent light-induced chromosome damageand its prevention in mouse cells in culture. In: Proceedings of the National Academy of Sciences of the UnitedStates of America, Jg. 75, H. 4, S. 1830–1833.Abstract Twenty-hour-exposure to fluorescent light produces chromatid breaks in a line of

adult mouse lung cells grown in Dulbecco-Vogt medium supplemented with fetalbovine serum. The light-induced damage appears to be enhanced by increasing theconcentration of oxygen in the gas phase of the culture. The effective wavelength(s)of light is in the visible range between 400 and 450 nm andis probably the mercuryemission peak at 405 or 436 nm. Addition of catalase or glutathione with ascorbicacid to the culture medium reduced the number of chromatid breaks to a level notsignificantly different from that in the shielded cultures. It thus appears that theproduction of H2O2 in the culture medium or in the cell is responsible for thechromatid breaks. Most of the chromosomal abnormalities observed in long-termculture of mouse cells may result from exposure of cells or medium to fluorescentroom lights in the presence of atmospheric oxygen. These genetic abnormalitiescan be minimized by shielding cells and medium from light, lowering the PO2 of themedium, and including reducing agents such as glutathione and ascorbic acid in themedium formulation.

Schlagwörter Ascorbic Acidpharmacology; Catalasemetabolism; Cells, Cultureddrugeffectsradiation effects; Chromosome Aberrations; Culture Media;Glutathionepharmacology; Hydrogen Peroxide; Light; Oxygen; Spectrum Analysis;Superoxide Dismutasemetabolism

Parshad, R.; Sanford, K. K.; Jones, G. M.; Tarone, R. E.; Hoffman, H. A.; Grier, A. H. (1981): Susceptibility tofluorescent light-induced chromatid breaks associated with DNA repair deficiency and malignant transformationin culture. In: Cancer research, Jg. 40, H. 12, S. 4415–4419.Abstract The increased susceptibility of mouse cells to fluorescent light-induced chromatid

damage following their spontaneous malignant transformation in culture could result

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavifrom loss or inactivation of catalase that decomposes the photoproduct H2O2 orfrom impaired capacities to repair DNA damage. No consistent change in catalaseactivity with respect to neoplastic state could be established. To interpret thecytogenetic damage in terms of DNA strand breaks, we determined the incidence ofchromatid breaks induced by light exposure during the G1 and late S-G2 phases ofthe cell cycle in normal and malignant derivatives of a C3H mouse cell line.Chromatid breaks at metaphase following light exposure during G1 would resultfrom DNA strand breaks, cross-links, or base damage, whereas breaks followingexposure during late S-G2 would result from single-or double-strand breaks. BothG1 and late S-G2 were susceptible in malignant cells but only G1 in normal. Sincecaffeine inhibits DNA repair, we compared its effects on light-induced chromatiddamage in the normal and malignant cells to assess their DNA repair capacities.Treatment of normal cells with caffeine (50 microgram/ml) directly following five hrof light exposure in G1 increased the chromatid damage to that in malignant cellsexposed with or without caffeine. Similarly, treatment of normal cells with caffeineduring late S-G2 exposure increased chromatid damage to a level not significantlydifferent from that in malignant cells exposed without caffeine. Caffeine had littleinfluence on chromatid damage in malignant cells. The increased susceptibility ofmalignant mouse cells to fluorescent light-induced chromatid breaks thus appearsto result from impaired capacities to repair DNA damage.

Schlagwörter Animals; Caffeinepharmacology; Catalasemetabolism; Cell Cycle; Cell Line; CellTransformation, Neoplasticmetabolism; Chromatidsradiation effects; ChromosomeAberrations; DNA Repair; Interphase; Light; Mice

Parshad, R.; Sanford, K. K.; Tarone, R. E.; Jones, G. M.; Baeck, A. E. (1979): Increased susceptibility of mousecells to fluorescent light-induced chromosome damage after long-term culture and malignant transformation. In:Cancer research, Jg. 39, H. 3, S. 929–933.Abstract Exposure of mouse cells in culture to fluorescent light has been shown to produce

chromatid breaks and exchanges. Hydrogen peroxide formed in the cell duringillumination has been implicated as the causative agent. The present resultsindicate that susceptibility to light-induced chromosome damage increases with timein culture and seems to be associated with or requisite for the spontaneousmalignant transformation of mouse cells. All three cell lines followed during long-term culture that either became tumorigenic or showed cytological evidence ofneoplastic transformation developed a concomitant increase in susceptibility. Inthree additional cell lines, susceptibility to light-induced chromatid damage wassignificantly increased in the spontaneously transformed malignant cells ascompared with their nonneoplastic precursors. The increased susceptibility is notsimply the result of long-term culture, since three other nonneoplastic cell lines afterprolonged culture were significantly less susceptible than their malignantcounterparts. Increased susceptibility to light-induced chromatid damage couldresult from impaired DNA repair or from the loss of defense mechanisms fordestroying H2O2 or scavenging free radicals.

Schlagwörter Animals; Cell Line; Cell Transformation, Neoplastic; Chromosome Aberrations;Crossing Over, Geneticradiation effects; DNAmetabolism; HydrogenPeroxidemetabolism; Lightadverse effects; Mice; Time Factors

Parshad, R.; Sanford, K. K.; Taylor, W. G.; Tarone, R. E.; Jones, G. M.; Baeck, A. E. (1980): Effect of intensityand wavelength of fluorescent light on chromosome damage in cultured mouse cells. In: Photochemistry andphotobiology, Jg. 29, H. 5, S. 971–975.Schlagwörter Animals; Catalasemetabolism; Cell Line; Chromatidsmetabolism;

Chromosomesradiation effects; Fluorescence; Hydrogen Peroxidemetabolism;Light; Mice

Pitts, D. G.; Bergmanson, J. P.; Chu, L. W. (1984): Rabbit eye exposure to broad-spectrum fluorescent light. In:Acta ophthalmologica. Supplementum, Jg. 159, S. 1–54.

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - CitaviAbstract Two F40CW fluorescent lamps mounted in an EYS-2404 fixture and 300 nm, 5 nm

waveband UV radiation were used to expose pigmented rabbit eyes. The results ofthe exposures to the eye were evaluated with the biomicroscope, ophthalmoscope,light microscope and electron microscope. The following conclusions were reached:The adverse ocular responses to fluorescent radiation exposure were due to long-duration, broadband radiation. These reactions were more generalized forfluorescent exposures when the cornea and lens are compared to UV exposures.The differences between the levels of threshold exposure needed to cause damagefor the fluorescent source and UV radiation were attributed to exposure durationand the rate of delivery of the radiation. Corneal and lenticular damage was mildwhen compared with UV 300 nm exposures, and the threshold occurred after 8 h to12 h of exposure. The effect of the radiation was to interfere with the normalfunctions of the cell while changes to the inert materials in the tissues wassecondary to injury to the cell. The damage was mild in the corneal epithelium,somewhat more severe in the corneal endothelium, but minimal in the cornealstroma. Early retinal changes were found after 8 h of exposure to the fluorescentsource. These induced changes were evident in the neural retina as spaces andwere assumed to represent oedema. The retinal oedema was initially found only inthe receptor cell, outer nuclear and nerve fibre layers. Many vacuoles or spaceswere located in the junctional area between the ganglion cell and nerve fibre layerswhile smaller spacing occurred also within the nerve fibre layer. Twelve h ofexposure to the fluorescent source produced a further increase in the oedema inthe retina. The outer segments of the receptor cells appear to disintegrate andsignificant open spaces are evident among the inner and outer segments of thereceptors. The inner plexiform layer shows an increased number of spaces withinand among the neural elements, and the mitochondria appeared to be undergoingchanges. The 20-h and longer exposure induced severe changes affecting all layersof the retina. These changes include massive retinal oedema with degenerativesigns in all retinal neurons. A sympathetic reaction of the unexposed, contralateraleye occurred as the result of the damage to the exposed eye. Minimal sympatheticresponses to the cornea and the lens began at exposure durations at or above 12h, while the retina showed the sympathetic reaction beginning at 8 h.(ABSTRACTTRUNCATED AT 400 WORDS)

Schlagwörter Animals; Cornearadiation effectsultrastructure; Eyeradiation effectsultrastructure;Fluorescence; Lens, Crystallineradiation effectsultrastructure; Lightadverse effects;Rabbits; Radiation Dosage; Time Factors; Ultraviolet Raysadverse effects

Reese, C. T.; Ntam, C.; Martin, T. V.; Carrington, S.; Leotaub, J.; Cox, L. et al. (2007): Internalization of near-infrared fluorescent dyes within isolated macrophage populations. In: Cellular and molecular biology (Noisy-le-Grand, France), Jg. 53, H. 3, S. 27–33.Abstract The development and application of microsensor technology has enhanced the

ability of scientists to further understand various biological activities, such aschanges in the intracellular environment after injury or toxic exposure. NIRmicrosensor technology may be useful in detecting the cellular injuries or adversechanges during the early onset period, allowing for the administration of therapies toinitiate recovery. The development and use of Infrared (IR) and near infrared (NIR)dyes as biological micro-sensors due to their advanced spectral characteristics maybe helpful. Three of the more useful NIR dye characteristics include the ability tominimize background interference by extraneous biological matrices, the ability toexhibit optimal molar absorptivity and quantum yields, and the ability to maintainnormal cellular activity. Thus, the current study was designed to investigate theability of selected NIR micro-sensor dyes to undergo cellular internalization,demonstrate intracellular NIR fluorescent signaling, and maintain normal cellularactivity. The results demonstrate that the selected NIR micro-sensor dyes undergocellular internalization. The presence of the dyes within the cells did not affect cellviability. In addition, these dyes demonstrate changes in absorbance and

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavifluorescence after the immune cells were challenged with a stimulant. Moreover,critical cellular functions, such as tumor necrosis factor release and superoxideproduction were not compromised by the internalization of the fluorescent dyes.These data suggest that selected NIR micro-sensor dyes can undergo intracellularinternalization within isolated macrophages without adversely affecting variousparameters of normal cellular activity.

Schlagwörter Analysis of Variance; Biological Transport; Biosensing Techniques; Chemotaxis;Fluorescent Dyes; Fluorometry; Infrared Rays; Macrophages; Spectrometry,Fluorescence; Superoxides; Tumor Necrosis Factor-alpha

Reinhardt, Harris (1942): The fluorescent lighting handbook. A practical guide to the performance,characteristics and applications of fluorescent lighting. Hygrade Sylvania corporation. (Hg.). Salem Mass.:Hygrade Sylvania Corporation.Schlagwörter Fluorescent lighting.

Reszka, K.; Eldred, G. E.; Wang, R. H.; Chignell, C.; Dillon, J. (1996): The photochemistry of human retinallipofuscin as studied by EPR. In: Photochemistry and photobiology, Jg. 62, H. 6, S. 1005–1008.Abstract Fluorescent material generated in the human retina accumulates within lipofuscin

(HLF) granules of the retinal pigment epithelium (RPE) during aging. We have beeninvestigating the possible light-induced contribution of these fluorophores to variousdiseases including age-related macular degeneration. Our studies have shown thatsome of the fluorescent components of HLF are products of the reaction ofretinaldehyde with ethanolamine and that synthetic mixtures of this reaction canserve as a useful model for photophysical studies. Previous research by us hasdemonstrated that irradiation of either natural or synthetic lipofuscin resulted in theformation of a triplet state and possibly a free radical. Here EPR studies wereperformed to verify the formation of that radical. The UV irradiation of eithersynthetic or natural human retinal lipofuscin extracts in oxygen-free methanol led tothe formation of a 5,5-dimethylpyrroline-N-oxide (DMPO) spin-trapped carbon-centered radical resulting from either hydrogen atom or electron abstraction fromsolvent molecules. In the presence of oxygen superoxide was formed, which wasobserved as a DMPO adduct. It is concluded that certain components of thechloroform-soluble fluorophores of human RPE lipofuscin granules and thefluorescent reaction products of retinaldehyde and ethanolamine arephotophysically similar but not the same. Electron or hydrogen abstraction from asubstrate by these fluorophores in vivo and the resulting radical products maycontribute to the age-related decline of RPE function and blue light damage in theretina.

Schlagwörter Adult; Electron Spin Resonance Spectroscopy; Humans;Lipofuscinchemistryisolation & purification; Photochemistry; Pigment Epithelium ofEyechemistrymetabolism

Saltarelli, C. G.; Coppola, C. P. (1979): Influence of visible light on organ weights of mice. In: Laboratory animalscience, Jg. 29, H. 3, S. 319–322.Abstract Hau:ICR mice separated by sex, were reared for 30 days under various fluorescent

lamps: pink, blue, black UV, cool white and full spectrum. Body weights andabsolute organ weights were compared. After light exposure, female body weightswere not significantly different between any groups; however, a difference in malebody weights was observed. Light affected the weights of the pituitary, adrenals,kidneys and prostate in male mice and the adrenals, thyroid and pineal glands infemales. The weight of adrenal glands of both males and females were mostsensitive to changes in lighting.

Schlagwörter Adrenal Glandsradiation effects; Animals; Body Weightradiation effects; Female;Light; Male; Micegrowth & development; Organ Sizeradiation effects; PinealGlandradiation effects; Pituitary Glandradiation effects; Sex Factors

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - CitaviSanford, K. K.; Parshad, R.; Jones, G.; Handleman, S.; Garrison, C.; Price, F. (1980): Role of photosensitizationand oxygen in chromosome stability and "spontaneous" malignant transformation in culture. In: Journal of theNational Cancer Institute, Jg. 63, H. 5, S. 1245–1255.Abstract Visible light and oxygen enhanced both chromosome instability and malignant

transformation of mouse cells in culture. Nine cell lines were initiated from 8 poolsof 10- to 13-day C3H embryos. Each cell line was divided into sublines, which wereeither maintained shielded from light or were exposed for 3 or 24 hours tofluorescent light (approximately 150 foot-candles) two or three times weekly.Cultures of the sublines were also maintained with either a gaseous phase of 0-1%oxygen or atmospheric (18%) oxygen. Each line was monitored for cytologicmanifestations of malignant neoplastic transformation, and 8 lines were monitoredfor chromosome alterations. Seven lines were assayed for tumorigenicity byintraocular implantation into syngeneic hosts. Repeated light exposure and/or highoxygen increased the frequency of minute chromosomes, which result fromchromatid breaks, and also increased the rate of shift from diploid to heteroploidstate. Four cell lines showed no cytologic changes indicative of neoplastic changeduring the test period. Two of these were assayed in vivo and failed to grow astumors. In the remaining 6 lines, cytologically neoplastic colonies appeared earlieror more abundantly in the light-exposed cultures and/or those gassed with highoxygen. In 3 of these lines, tumors developed only from the light-exposed cultures;in the other 2, tumor latency periods were significantly shorter in the culturesexposed to light or gassed with atmospheric oxygen.

Schlagwörter Animals; Cell Divisionradiation effects; Cell Line; Cell Survivalradiation effects; CellTransformation, Neoplastic; Chromosome Aberrations; Embryo, Mammalian;Lightadverse effects; Mice; Mice, Inbred C3H; Neoplasm Transplantation;Neoplasms, Experimentaletiology; Oxygen; Transplantation, Homologous

Schmidt, Tiffany M.; Taniguchi, Kenichiro; Kofuji, Paulo (2008): Intrinsic and extrinsic light responses inmelanopsin-expressing ganglion cells during mouse development. In: Journal of neurophysiology, Jg. 100, H. 1,S. 371–384. Online verfügbar unter doi:10.1152/jn.00062.2008.Abstract Melanopsin (Opn4) is a photopigment found in a subset of retinal ganglion cells

(RGCs) that project to various brain areas. These neurons are intrinsicallyphotosensitive (ipRGCs) and are implicated in nonimage-forming responses toenvironmental light such as the pupillary light reflex and circadian entrainment.Recent evidence indicates that ipRGCs respond to light at birth, but questionsremain as to whether and when they undergo significant functional changes. Weused bacterial artificial chromosome transgenesis to engineer a mouse line in whichenhanced green fluorescent protein (EGFP) is expressed under the control of themelanopsin promoter. Double immunolabeling for EGFP and melanopsindemonstrates their colocalization in ganglion cells of mutant mouse retinas.Electrophysiological recordings of ipRGCs in neonatal mice (postnatal day 0 [P0] toP7) demonstrated that these cells responded to light with small and sluggishdepolarization. However, starting at P11 we observed ipRGCs that responded tolight with a larger and faster onset (<1 s) and offset (<1 s) depolarization. Thesefaster, larger depolarizations were observed in most ipRGCs by early adult ages.However, on application of a cocktail of synaptic blockers, we found that all cellsresponded to light with slow onset (>2.5 s) and offset (>10 s) depolarization,revealing the intrinsic, melanopsin-mediated light responses. The extrinsic,cone/rod influence on ipRGCs correlates with their extensive dendritic stratificationin the inner plexiform layer. Collectively, these results demonstrate that ipRGCsmake use of melanopsin for phototransduction before eye opening and that thesecells further integrate signals derived from the outer retina as the retina matures.

Schlagwörter Action Potentialsphysiologyradiation effects; Age Factors; Animals; Animals,Newborn; Chromosomes, Artificial, Bacterialphysiology; Dose-ResponseRelationship, Radiation; Gene Expression Regulation,Developmentalphysiologyradiation effects; Green Fluorescent

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - CitaviProteinsgeneticsmetabolism; Light; Mice; Mice, Transgenic; Patch-ClampTechniquesmethods; Photic Stimulationmethods; Reaction Time;Retinacytologygrowth & development; Retinal Ganglion Cellsmetabolismradiationeffects; Rod Opsinsgeneticsmetabolism

Sheng, Hui; Lu, Yi; Qing, Feng-ling (2008): [Blue light-induced damage to human retinal pigmented epithelialcells mediated by A2E]. In: [Zhonghua yan ke za zhi] Chinese journal of ophthalmology, Jg. 43, H. 11, S.1017–1021.Abstract OBJECTIVE: To observe the internalization of A2E by human retinal pigmented

epithelial (hRPE) cells and study whether the lipofuscin fluorophore A2E (N-retinylidene-N-retinylethanolamine) participates in blue light-induced damage tohRPE cells. METHODS: A mixture of all-trans-retinal and ethanolamine was used toproduce A2E in one step. A2E granules were delivered to medium of cultured hRPEcells for internalization. Confluent cultures were subsequently exposed to 450 nm(blue) light for 20 minutes with or without A2E (25, 50, 100 micromol/L). The lightintensity was 70 mW/mm(2). Phototoxicity was quantified at 12, 24, 36, and 48 hafter exposure by CCK-8 of viable cells. Apoptosis of cells was detected by Hoechst33342 DNA staining and flow cytometry. RESULTS: The reaction of all-trans-retinal(100 mg) and ethanolamine (9.5 mg) produced 53.8 mg A2E in one step. WhenA2E was delivered to hRPE cells in culture, it accumulated intracellularly.Internalized A2E presented as autofluorescent granules having a perinucleardistribution. As shown by CCK-8 analysis, the A2E-fed hRPE cell viability reducedwith duration after 450 nm light exposure. Conversely, blue light-exposed hRPEcells that did not contain A2E showed less loss of cell viability. The percentage ofhRPE cell apoptosis with 25 micromol/L A2E 12, 24, 36 and 48 h after blue lightexposure was (12.11 +/- 2.32)%, (31.21 +/- 3.72)%, (64.23 +/- 3.53)% and (58.71+/- 3.48)% respectively. Conversely, the apoptosis was less than 5% in other hRPEcells. CONCLUSIONS: A2E is essential to blue light-induced hRPE cell damage.Only blue light exposure and without A2E lead to little cell injury. hRPE cells in oldpeople which contain much lipofuscin are sensitive to blue light injury.

Siopes, T. D. (1984): The effect of full-spectrum fluorescent lighting on reproductive traits of caged turkey hens.In: Poultry science, Jg. 63, H. 6, S. 1122–1128.Abstract Large White turkey breeder hens were exposed to either incandescent or full-

spectrum (FS) fluorescent lighting during two 20-week reproductive cycles in closedconfinement. Data were recorded for body weights, feed intake, and reproductivetraits. Body weights and feed intake were similar between treatments in both egglaying cycles. In addition, there were no significant differences in egg production,fertility, hatchability, or poult weight between the incandescent and FS fluorescentlight treatment in either the first or second year egg laying cycle. It was concludedthat exposure of breeder turkey hens to FS fluorescent light in closed confinementresults in reproductive performance similar to that obtained with incandescentlighting.

Schlagwörter Animals; Body Weight; Eating; Female; Fluorescence; Housing, Animal; Light;Oviposition; Reproduction; Turkeysphysiology

Society for Visual Education. (Hg.) (1970): "Cool" light from electricity (Filmstrip). n.p.: Society for VisualEducation.Schlagwörter Electric currents.; Neon lamps.; Fluorescent lighting.

Spreadbury, F. G. (1946): Electric discharge lighting. London: Sir I. Pitman & sons ltd.Schlagwörter Electric lighting, Mercury vapor.; Electric lighting, Sodium vapor.; Fluorescent

lighting.

Stark, W. S.; Carlson, S. D. (1985): Blue and ultraviolet light induced damage to the Drosophila retina:ultrastructure. In: Current eye research, Jg. 3, H. 12, S. 1441–1454.

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - CitaviAbstract Intense ultraviolet (UV) and blue stimulation photolyses rhodopsin through a

fluorescent metarhodopsin (M') in the predominant photoreceptor type, R1-6, of thecompound eye of white eyed Drosophila melanogaster. We investigated theassociated retinal degeneration using High Voltage Electron Microscopy (HVEM).The threshold for UV induced damage was about 19 log quanta/cm2 while for blue,the threshold was about 20. These intensities are toward the upper level of thedynamic range for rhodopsin photolysis. Thus, there is a sensitization for near UVinduced degeneration as had been found for photolysis of the visual pigment.Vitamin A deprivation protects against light elicited retinal degeneration, particularlyin the UV. Since vitamin A deprivation eliminates the blue absorbing rhodopsin anda UV sensitizing pigment in R1-6, the degeneration is likely mediated throughquantal absorption through these photoexcitation pigments. Intense light convertsthe microvilli of the rhabdomeres (the photopigment containing organelles) intodense strands and the cytoplasm fills with a dense reticulum. Such damage iselicited shortly after stimulation and is permanent. Under most conditions, thesecond order interneurons are spared. These results are discussed in the context ofother animal models of intense light retinal degeneration.

Schlagwörter Animals; Dose-Response Relationship, Radiation; Drosophila melanogaster;Interneuronsradiation effects; Microscopy, Electron; Neurogliaradiation effects;Neuronsradiation effects; Photoreceptor Cellsradiation effects; Radiation Injuries,Experimentaletiologypathology; Retinapathologyradiation effects; RetinalDegenerationetiologypathology; Synapsesradiation effects; Ultraviolet Raysadverseeffects

Stark, W. S.; Walker, K. D.; Eidel, J. M. (1985): Ultraviolet and blue light induced damage to the Drosophilaretina: microspectrophotometry and electrophysiology. In: Current eye research, Jg. 4, H. 10, S. 1059–1075.Abstract Intense ultraviolet (UV) and blue stimulation decreases visual pigment

concentration and increases long wavelength fluorescent emission in R1-6photoreceptors in the white eyed fruit fly Drosophila melanogaster. We usedmicrospectrophotometry to show that the threshold for visual pigment decrease isabout 1 log unit lower for UV than for blue light (18.7 vs approximately 19.9 logquanta/cm2 respectively). UV and blue stimuli about 0.2 log units brighter had beenshown to cause structural degeneration. Above the threshold for structural damage,visual pigment is decreased permanently while below this level, a recovery of visualpigment was achieved within several hours. Microspectrofluorometric data arepartially consistent with the hypothesis that the visual pigment is converted into afluorescent product which had been named M'. M' had been proposed to be a newform of metarhodopsin which absorbs chiefly in the yellow and which has afluorescent emission in the red; long wavelength stimulation had been reported toregenerate the native visual pigment from M'. Our data suggest that the situation issignificantly more complex than this simple model. For instance, we report that longwavelength stimulation regenerates only a small fraction of the visual pigment whichhad been decreased by UV or blue stimulation. Furthermore, several lines ofevidence suggest that other fluorescent products are also created by intense UVand blue stimulation. We were particularly interested in the lower damage thresholdfor UV light because of the hypothesis that UV visual sensitivity is mediated by asensitizing pigment which absorbs UV light and transfers its energy to the blueabsorbing rhodopsin. Our data suggest that the UV light decreases the rhodopsinwithout preferentially decreasing the sensitizing pigment.

Schlagwörter Animals; Drosophila melanogasterradiation effects; Electrophysiology;Electroretinography; Fluorometry; Lightadverse effects; Retinaradiation effects;Retinal Pigmentsbiosynthesismetabolismradiation effects;Spectrophotometrymethods; Time Factors; Ultraviolet Raysadverse effects

Stenkamp, Deborah L.; Satterfield, Rosanna; Muhunthan, Kalyani; Sherpa, Tshering; Vihtelic, Thomas S.;Cameron, David A. (2008): Age-related cone abnormalities in zebrafish with genetic lesions in sonic hedgehog.

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - CitaviIn: Investigative ophthalmology & visual science, Jg. 49, H. 10, S. 4631–4640. Online verfügbar unterdoi:10.1167/iovs.07-1224.Abstract PURPOSE: Sonic hedgehog (Shh) signaling is essential for photoreceptor

differentiation and retinal cell survival in embryonic zebrafish. The study wasconducted to determine whether adult heterozygous carriers of mutant alleles forthe shh gene display retinal abnormalities. METHODS: Retinal cryosections fromyoung, middle-aged, and senescent wild-type and sonic-you(+/-) (syu(+/-)) zebrafishwere probed with retinal cell type-specific markers. Contralateral retinal flatmountsfrom these fish, and from adult albino zebrafish subjected to light-inducedphotoreceptor damage followed by regeneration, were hybridized with blue coneopsin cRNA for quantitative analysis of the blue cone pattern. Retinal expression ofshh mRNA was measured by quantitative RT-PCR. RESULTS: Regions of coneloss and abnormal cone morphology were observed in the oldest syu(+/-) zebrafish,although no other retinal cell type was affected. This phenotype was age-relatedand genotype-specific. Cone distribution in the oldest syu(+/-) zebrafish waspredominantly random, as assessed by measuring the short-range pattern, whereasthat of wild-type fish and the younger syu(+/-) zebrafish was statistically regular. Ameasure of long-range pattern revealed atypical cone aggregation in the oldestsyu(+/-) zebrafish. The light-treated albino zebrafish displayed random conepatterns immediately after light toxicity, but showed cone aggregation onregeneration. Retinas from the syu(+/-) fish showed reduced expression of shhmRNA compared with those of wild-type siblings. CONCLUSIONS: The syu(+/-)zebrafish presents a model for the study of hereditary age-related coneabnormalities. The syu(+/-) retinas most likely experience progressive conephotoreceptor loss, accompanied by cone regeneration. Shh signaling may berequired to maintain cone viability throughout life.

Schlagwörter Agingphysiology; Alleles; Animals; Cell Death; Cell Proliferation; FluorescentAntibody Technique, Indirect; Gene Expressionphysiology; HedgehogProteinsgenetics; In Situ Hybridization; In Situ Nick-End Labeling; Light;Microscopy, Fluorescence; Mutation; RNA, Messengermetabolism; RadiationInjuries, Experimentaletiologygeneticspathology; Retinaradiation effects; RetinalCone Photoreceptor Cellsmetabolismpathology; RetinalDegenerationetiologygeneticspathology; Reverse Transcriptase Polymerase ChainReaction; Rod Opsinsmetabolism; Zebrafishgenetics; Zebrafish Proteinsgenetics

Stoutemyer, Vernon Theodore; Close, Albert William (1945): Plant propagation under fluorescent light. UnitedStates. (Hg.). Beltsville Md.Schlagwörter Plant propagation.; Fluorescent lighting.

Strum, Carl Heinz (1952): Vorschaltgeräte und Schaltungen für Leuchtstofflampen. Brown, Boveri &. Cie A. -G(Hg.). Mannheim: Brown Boveri & Cie.Schlagwörter Fluorescent lighting.

Taniguchi, Yukinori; Ikehara, Tatsuya; Kamo, Naoki; Watanabe, Yasutaka; Yamasaki, Hiroshi; Toyoshima,Yoshinori (2007): Application of fluorescence resonance energy transfer (FRET) to investigation of light-inducedconformational changes of the phoborhodopsin/transducer complex. In: Photochemistry and photobiology, Jg.83, H. 2, S. 311–316. Online verfügbar unter doi:10.1562/2006-06-15-RA-922.Abstract The photoreceptor phoborhodopsin (ppR; also called sensory rhodopsin II) forms a

complex with its cognate the Halobacterial transducer II (pHtrII) in the membrane,through which changes in the environmental light conditions are transmitted to thecytoplasm in Natronomonas pharaonis to evoke negative phototaxis. We haveapplied a fluorescence resonance energy transfer (FRET)-based method forinvestigation of the light-induced conformational changes of the ppR/pHtrII complex.Several far-red dyes were examined as possible fluorescence donors or acceptorsbecause of the absence of the spectral overlap of these dyes with all thephotointermediates of ppR. The flash-induced changes of distances between the

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavidonor and an acceptor linked to cysteine residues which were geneticallyintroduced at given positions in pHtrII(1-159) and ppR were determined from FRETefficiency changes. The dye-labeled complex was studied as solubilized in 0.1% n-dodecyl-beta-D-maltoside (DDM). The FRET-derived changes in distances fromV78 and A79 in pHtrII to V185 in ppR were consistent with the crystal structure data(Moukhametzianov, R. et al. [2006] Nature, 440, 115-119). The distance from D102in pHtrII linker region to V185 in ppR increased by 0.33 angstroms upon the flashexcitation. These changes arose within 70 ms (the dead time of instrument) anddecayed with a rate of 1.1 +/- 0.2 s. Thus, sub-angstrom-scale distance changes inthe ppR/pHtrII complex were detected with this FRET-based method using far-redfluorescent dyes; this method should be a valuable tool to investigate conformationchanges in the transducer, in particular its dynamics.

Schlagwörter Archaeal Proteins; Fluorescence Resonance Energy Transfer; Halobacteriaceae;Halorhodopsins; Multiprotein Complexes; Photochemistry; Protein Conformation;Recombinant Proteins; Sensory Rhodopsins

Tanito, Masaki; Kaidzu, Sachiko; Anderson, Robert E. (2006): Protective effects of soft acrylic yellow filteragainst blue light-induced retinal damage in rats. In: Experimental eye research, Jg. 83, H. 6, S. 1493–1504.Online verfügbar unter doi:10.1016/j.exer.2006.08.006.Abstract Recently, a yellow intraocular lens (IOL) was developed for the purpose of reducing

potential blue light-induced retinal damage after cataract surgery. However, theeffect of yellow filters on retinal protection remains to be clarified. To test theprotective effects of yellow filters on blue light-induced retinal damage, a yellow anda clear soft acrylic filter were attached to the right and left eyes, respectively, ofalbino rats and exposed to 4.5 k lux blue fluorescent lights with peak wavelength at420 nm (ranging 380-500 nm; short blue) or 446 nm (ranging 400-540 nm; longblue) for 6h. To assess retinal damage, the electroretinogram (ERG) was recordedat 7 days, outer nuclear layer (ONL) thickness and area were measured at 7 days,apoptosis was analyzed by TUNEL staining at 24 h, and the level of lipidperoxidation in retinas was assessed by Western dot blots using specific antibodiesagainst 4-hydroxynonenal (4-HNE)- and carboxyethylpyrrole (CEP)-modifiedproteins immediately after light exposure. After short blue light exposure, a- and b-wave ERG amplitudes and the ONL thickness at 1-2.5 mm inferior and 0.5-2.5 mmsuperior to optic nerve head (ONH) were significantly reduced. TUNEL staining inthe ONL at 0-2 mm inferior and 1-2 mm superior to the ONH, and retinal levels of 4-HNE- and CEP-modified proteins were significantly increased in the clear filter-covered eyes compared to yellow filter-covered eyes. After long blue light exposure,the only difference seen was a greater ONL thickness at 1.5 mm superior to theONH in yellow filter-covered eye. Transmission of light through the yellow filter was58% for short blue and 89% for long blue compared to the clear filter. The ONL areawas not different between clear filter-covered and -uncovered eyes after exposureto short or long blue light. Given the results, yellow IOL material protects the retinaagainst acute shorter wavelength blue light exposure more effectively than the clearIOL material.

Schlagwörter Animals; Apoptosisradiation effects; Color; Electroretinography; EyeProteinsmetabolism; Filtrationinstrumentation; Lens, Crystallinephysiologyradiationeffects; Lightadverse effects; Lipid Peroxidation; Photoreceptor Cells,Vertebrateradiation effects; Radiation Injuries, Experimentalprevention & control;Rats; Rats, Sprague-Dawley; Retinametabolismphysiopathologyradiation effects;Retinal Degenerationpathologyprevention & control; Scattering, Radiation;Ultraviolet Rays

Veitch, J. A.; McColl, S. L. (2001): A critical examination of perceptual and cognitive effects attributed to full-spectrum fluorescent lighting. In: Ergonomics, Jg. 44, H. 3, S. 255–279.Abstract Full-spectrum fluorescent lighting (FSFL) has been credited with causing dramatic

improvements in vision, perception and cognitive performance as compared with

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citaviother fluorescent lamp types. These effects are hypothesized to occur because ofsimilarity between FSFL emissions and daylight, which is said to have evolutionarysuperiority over other light sources. This review, covering 1945-98, criticallyconsiders the evidence for these claims. In general, poor-quality research hasresulted in an absence of simple deterministic effects that can be confidentlyattributed to fluorescent lamp type. Promising avenues for lighting behaviourresearch include investigations of cognitive mediators of lighting-behaviourrelationships, and flicker rates and colour rendering effects on visual processing,appearance judgements and affect. Good lighting solutions are more complex thanlamp type specification.

Schlagwörter Cognition; Humans; Job Satisfaction; Lighting; Task Performance and Analysis;Visual Perception; Workplace

Wyse, J. P. (1980): Renewal of rod outer segments following light-induced damage of the retina. In: Canadianjournal of ophthalmology. Journal canadien d'ophtalmologie, Jg. 15, H. 1, S. 15–19.Abstract Fluorescent lighting was used to induce severe but reversible damage of the rod

outer segments of the retinas of albino rats. The animals were then kept incontinuous darkness for up to 12 days. Pairs of animals were killed after 1, 3, 5, 7, 9and 12 days of continuous darkness. Light microscopic examination of the retinasdemonstrated a sharp demarcation between the light-damaged distal ends of therod outer segments and the newly formed proximal ends. Measurement of theproximal ends demonstrated proximo-distal renewal of the rod outer segmentsduring the first 9 days of continuous darkness. Parametric statistical analysis of thedata revealed that the renewal occurred linearly, at an average rate of 2.66micron/d, which is similar to the rate of renewal of the rod outer segments in theundamaged retina of the rat.

Schlagwörter Animals; Dark Adaptation; Lightadverse effects; PhotoreceptorCellsphysiologyradiation effects; Rats; Regeneration

Xu, Xiaoyang; Zhao, Xiufeng; Liu, Timon Cheng-Yi; Pan, Hongying (2008): Low-Intensity Laser IrradiationImproves the Mitochondrial Dysfunction of C2C12 Induced by Electrical Stimulation. In: Photomedicine and lasersurgery. Online verfügbar unter doi:10.1089/pho.2007.2125.Abstract Abstract Objective: We investigated the effects of electrical stimulation and low-

intensity laser (LIL) energy on the mitochondrial function of cultured C2C12myotubes in order to find a dosage that could be used to improve the function ofmitochondria, and then rehabilitate exercise-induced damage and fatigue.Background Data: Many other studies in the past demonstrated that LIL had acytoprotective effect, and a recent study also found that LIL could reduce muscularfatigue during tetanic contractions in rats. Methods: Cultured C2C12 myotubes weresubjected to electrical stimulation or/and LIL irradiation at various intensities.Reactive oxygen species (ROS) were detected with a fluorescent probe (DCFH-DA)and mitochondrial function was assessed with an MTT assay. Results: The resultsshowed that electrical stimulation at 20 ms, 5 Hz, and 45 V for 75 min can inducemitochondrial dysfunction in cultured C2C12 myotubes. Electrical stimulation-induced mitochondrial dysfunction was improved, but degeneration occurred withLIL at doses of 0.33-8.22 and 11.22-14.16 J/cm(2), respectively, and these changeswere markedly increased with LIL at 0.33 and 1.34 J/cm(2), respectively.Conclusions: We conclude that treatment of myotubes with the proper dosage ofLIL irradiation significantly diminished production of ROS and restoredmitochondrial function, and this may provide a foundation for the use ofphotobiomodulation to treat exercise-induced mitochondrial dysfunction or skeletalmuscular fatigue.

Yu, Xiaoping; Chen, Ka; Wei, Na; Zhang, Qianyong; Liu, Jihuan; Mi, Mantian (2007): Dietary taurine reducesretinal damage produced by photochemical stress via antioxidant and anti-apoptotic mechanisms in Sprague-Dawley rats. In: The British journal of nutrition, Jg. 98, H. 4, S. 711–719. Online verfügbar unter

iLib08 - CitaviiLib08 - CitaviiLib08 - CitaviiLib08 - Citavidoi:10.1017/S0007114507744409.Abstract Taurine has been shown to be tissue protective in many models of oxidant-induced

injury. However, its protective role against retinal damage induced byphotochemical stress is less well known. The purpose of the present study was toinvestigate whether dietary taurine reduced retinal photochemical damage inSprague-Dawley rats and to further explore the underlying molecular mechanismsof this action. Twenty rats fed AIN-93 formulation and maintained in the dark for 48h were used as controls (n 20). Another forty rats were randomly divided into twogroups and then treated with (n 20) or without 4 % taurine (n 20) for 15 drespectively. After treatment, these two groups were exposed to fluorescent light(3000 +/- 200 lux and 25 degrees C), and the protective effects of dietary taurinewere then evaluated. The present results showed that dietary taurine effectivelyprevented retinal photochemical damage as assessed by changes of morphology.Also, the supplementation caused an increase of taurine in the retina, a decrease ofmalondialdehyde (P < 0.01), and elevation of superoxide dismutase (P < 0.01) andglutathione peroxidase activities in the retina (P < 0.01). Moreover, dietary taurineinhibited activator protein-1 (AP-1) (c-fos/c-jun subunits) expression (P < 0.05), upregulated NF-kappaB (p65) expression (P < 0.05), and decreased caspase-1expression (P < 0.05) so as to reduce the apoptosis of photoreceptors in the retina(P < 0.05). These results suggest that dietary taurine reduced retinal damageproduced by photochemical stress via antioxidant and anti-AP-1-NF-kappaB-caspase-1 apoptotic mechanisms in rats.

Schlagwörter Animals; Antioxidantsphysiology; Apoptosisdrug effects; Diet; Oxidants,Photochemicalpharmacology; Random Allocation; Rats; Rats, Sprague-Dawley;Retinal Diseaseschemically inducedprevention & control; Taurineadministration &dosagepharmacology; Treatment Outcome

Zand, M. S.; Albrecht-Buehler, G. (1989): Long-term observation of cultured cells by interference-reflectionmicroscopy: near-infrared illumination and Y-contrast image processing. In: Cell motility and the cytoskeleton,Jg. 13, H. 2, S. 94–103. Online verfügbar unter doi:10.1002/cm.970130204.Abstract Interference-reflection microscopy (IRM) is the only method presently available with

which to visualize cell-substratum adhesions in living tissue culture cellscontinuously for long periods of time without the use of fluorescent markers (Curtis:J. Cell Biol. 20:199-215, 1964; Izzard and Lochner: J. Cell Sci. 21:129-159, 1976).This method utilizes approximately 1% of the incident illumination to produce theIRM image (Verschueren: J. Cell Sci. 75:279-301, 1985) and so far has required theuse of high-intensity light sources in the visible spectral range (400-800 nm).Unfortunately, visible light of this intensity and spectral range induces markedchanges in the behavior and morphology of motile fibroblasts, including cessation oflocomotion. In contrast, the present paper reports that continuous observations oflive cells in IRM for periods of up to 8 hours are possible if the illuminating light is inthe red to near-infrared range (650-950 nm) and without any observable change innormal cell morphology or behavior. In addition, we describe how the technique ofY-contrast image processing can be applied to IRM images to create a three-dimensional image of the ventral cell surface topography.

Schlagwörter Animals; Cell Line; Cell Movement; Cells, Cultured; Fibroblasts; Infrared Rays;Mice; Microscopy, Interference

Zwikker, C. (1952): Fluorescent lighting. A review of the scientific and technical fundamentals and of theapplications of the fluorescent lamp and its accessories. London: distributors for United Kingdom; Cleaver HumePress; distributors for U.S.A.: Elsevier Press Houston (Philips technical library).Schlagwörter Fluorescent lighting.