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The Oxidative Stress in Cataract Patients

INTRODUCTIONTurbidity partial or total well represented in

lens cause visual disturbancesThe reversible cause blindness in the world

todayFactors involved in the process karaktogenesis

(jj harding) :o Defense Antioxidant Capacity Lowo Lipid Peroxidation Higho Addition Glikolisasi Non-enzymatico Reduced Function Coach Of Alfa Cristalino Increased Permeability Occurrence Of Membrane

Lens

METHODS

50 patients with cataracts, age range 45-75 years, which is an outpatient Eye Hospital Department of Ram Lal, Medical College, Amritsar, India

A group of 50 healthy people who have the same age, originating from the same population, acting as controls

During the selection of subjects from both groups :-ensure that no history of chronic disease or metabolic disorders earlier- Cataract diagnosis is made by an eye doctor after a complete eye examination- Patients who used drugs were excluded from the study of antioxidants

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After getting approval in writing

DECISION ON THE SUBJECT OF BLOOD VENA

RESULTS

Serum MDA LevelsEstimated mean serum MDA levels in cataract patients and controls was 5.43 ± 1.69 nmol / ml and 2.42 ± 0.46 nmol / ml.

Serum concentrations of lipid peroxides in the form of MDA was significantly higher in patients with cataract (p <0.001) compared with the control

group

Serum Sod Levels The average serum concentrations of superoxide dismutase in patients with cataract and control groups respectively, was 2.75 ± 0.40 units / ml and 4.25 ± 1.20 units / ml.

The levels of antioxidant enzymes, SOD significantly decreased in patients with

cataracts compared with the control group

Blood Glutathione Peroxidase Levels

Glutathione peroxidase levels on average in the blood in patients with cataract was 29.23 ± 11.90. GPX levels in the control group was 70.29 ± 10:53.

SGPT levels in blood decreased in patients with cataracts compared with the control group. Obtained statistically significant reduction

DISCUSSION

Eye lens is continuously exposed to light and oxygen at high risk for damage photoxidative resulting in cataracts.

The onset of oxygen free radicals not only damage the crystalline lens aggregate and berpresipitat, causing turbidity, but also produce proteolytic enzymes that function to eliminate damaged proteins.

Regardless of the enzymatic defense system consisting of superoxide dismutase, catalase and glutathione peroxidase against the active oxygen species, the lenses containing the antioxidant vitamins C and E and beta-carotene might as other defense mechanisms.

The underlying pathophysiology of age-related cataracts are complex and not fully understood. It is believed that the oxidation is an event that started the whole sequence of processes that occur that cause cataracts

Oxidative stress can be caused by an imbalance between the production of reactive oxygen species and cellular antioxidant defense mechanisms. In the eye cells, reactive oxygen species initiating radical chain reactions that lipid peroxidation of membranes and damage to proteins, which cause intracellular protein aggregation and precipitation.

Lipid peroxidation produce tissue oxidative damage caused by hydrogen peroxide, superoxide anion and hydroxyl radicals, causing changes in membrane structure, with the contents of the cell and organelle expenses and loss of cytosolic aldehyde and peroxide products. Malenaldehyde is the main end products of free radical reactions in the membrane fatty acids.

In our study, the increase in MDA levels seen in Table 1, which indicates increased oxidative stress or a decrease in antioxidant defense mechanisms. In the case of development of age-related cataracts, LPO also can be a real cause of the destruction of the plasma membrane of the fiber lenticular lens oligomerization of Crystal (16). Lipid peroxidation can be associated with premature development of senile cataract (17). Therefore, it can be stated that the LPO is one of the possible causes of the development of cataracts.

SOD is an enzymatic antioxidant which is the first line of defense that acts as a reducer of reactive oxygen and convert it into H2O2. Perhaps there are two reasons why there is a decrease SOD:o Due to the increasing number of ROS such as

reactive oxygen species that are produced, SOD will be used more in converting oxygen into H2O2

o H2O2 also causes inhibition of SOD activity. There are several classes of SOD have different abilities to bind the metal, which is distributed in different cellular compartments and sensitivity to various reagents.

The study also showed a decrease in the activity of glutathione peroxidase related to age (Table 3). Results of this study confirm previous findings related cataracts in humans (22). Which suggests that the decrease in erythrocyte antioxidant status may increase oxidative damage in tissues, which include oxidative modification of proteins that occur in cataract lens. However, in contrast to these data, the levels of antioxidant enzymes in the blood are reported to have a relationship with cataracts (22-24).

CONCLUSIONOxidative stress on the lens has a direct

influence on the solubility of the lens proteins, which causes an increase in clouding of the lens.

Antioxidant enzyme activity reflect changes that occur in the development of senile cataract.

Testing of plasma TBARS levels of enzymes and can be used as a sign of the degeneration of the lens

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