Vitamin E,Vitamin C And Scurvy

BY DR.RISHAV RAJ

INTRODUCTION

Vitamin E is naturally occuring anti-oxidant.

It is known as “anti-sterility vitamin” because it helps in normal reproduction in many animals.

Vitamin E is a Fat soluble vitamin. Also known a beauty vitamin

HISTORY

1922: Evans and Bishop, described Vitamin E deficiency

1936: Evans et al, Isolated α-tocopherol 1960s: Vitamin E deficiency was described

in children with fat mal absorption syndromes.

1980s: Major symptom of vitamin E deficiency in Human was a peripheral neuropathy.

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STRUCTURE

CHEMISTRY

Vitamin E is the name given to a group of toco pherols and tocotrienols.

Till now 8 tocopherols have been identified alpha ,beta, gamma,delta..etc

Among this alpha tocopherol is active. Tocopherols are derivatives of 6-

hydroxy chromane The anti –oxidant property is due to

chromane ring.

Metabolism

Dietary tocopherol is dissolved in fats.

Absorbed in cell membrane ---distributed to peripheral tissue------cell membrane remant----liver----transported in VLDL----------------STORED IN ADIPOSE TISSUE.

BIOCHEMICAL FUNCTIONS 1.Vitamin E is essential for the membrane

structure and integrity of the cell ,hence it is regarded as a membrane antioxidant.

2.It prevents the peroxidation of PUFA in various tissues and membranes .it prevents RBC from hemolysis by oxidizing agents eg.. Hydrogenperoxide.

3.It is closely associated with reproductive functions and prevents sterility. vit.E preserves and maintains germinal epithelium of gonads for proper reproductive function.

4.Vitamin E protects liver from being damaged by toxic compounds such as carbon tetrachloride.

5.It works in association with vitamin A,C and beta carotene to delay the onset of cataract.

6.RECENT studies have shown that high intake of vitamin E protects against the development of heart diseases.It is believed that vit E prevents oxidation of LDL. The oxidised LDL Have been implicated to promote heart diseases .

Vitamin E and cancer

Vitamin E also inhibits the conversion of nitrites in the stomach to nitrosamines, which are cancer promoters.

RECOMMENDED DIETARY ALLOWANCE (RDA)

A daily consumption of 10 mg (15 IU) of alpha tocopherol for man.

8mg 12 IU for woman is recommended 1mg of alpha tocopherol =1.5 IU. Vitamin E supplement is advised for

pregnant and lactating women.

Ref:horwitt m.k, critique of the req.for vit e.Am.J.CLIN nutr.2001,73:1003-1005

Dietary sources

• Eggs• Milk• Nuts, such as almonds • Spinach and other green leafy vegetables• Unheated vegetable oils• Wheat germ• Wholegrain foods

• Ref:harper’s biochemistry

Who…

• People more than 55 years of age• Very low birth weight infants• Those who abuse alcohol and other drugs•  Those with: 

o cystic fibrosis o celiac diseaseo hyperthyroidismo malnutrition o liver, gallbladder, or pancreatic disease

o Ref: harper’s biochemistry..

Clinical manifestation

A severe ,progressive neurological disorder.

Loss of deep tendon reflexes Limb ataxia Dysarthria Ophthalmoplegia Nystagmus Positive romberg test Edema in premature infant and hemolysis

 Ataxia with vitamin E deficiency

Vitamin E is an antioxidant that protects cells in the body from the damaging effects of unstable molecules called free radicals. Lack of vitamin E causes neurological problems, such as difficulty coordinating movements (ataxia) and speech (dysarthria), loss of reflexes in the legs , and a loss of sensation in the extremities (peripheral neuropathy).

How common is ataxia with vitamin E deficiency?

Ataxia with vitamin E deficiency is a rare condition; however, its prevalence is unknown

Genes are related to ataxia with vitamin E deficiency

Mutations in the T T PA gene cause ataxia with vitamin E deficency.

The TTPA gene provides instructions for making the α-tocopherol transfer protein (αTTP), which is found in the liver and brain.

 This protein controls the distribution of vitamin E obtained from the diet (also called α-tocopherol) to cells and tissues throughout the body.

Cells neutralize free radicals with the aid of vitamin E, which prevents damage to the cell. Mutations in the TTPA gene impair the activity of the αTTP protein, resulting in an inability to retain and use dietary vitamin E. This deficiency leads to accumulation of free  radicals within cells

Role of vitamin E in the nutrition ofpremature infants

Vitamin E (a-tocopherol) has been credited with a variety of beneficial effects in

the premature newborn infant.

It has been thought that deficiency of vitamin E is at least partly responsible for the anemia which often occurs 4 to 6 wk after premature birth, and routine dietary supplementation with vitamin E is frequently recommended.

In NEWBORN vitamin E acts free radical scavenger and natural anti-oxidant that

Protects the cell membranes against lipid peroxidation.

REQUIRED FOR PREMATURE BABY:Because there is a significant transfer of

vitamin E during the last trimester of pregnancy.so , vitamin E is required for preventing haemolysis ,edema and anaemia

Lab findings

Serum vit E LEVEL increases in presences of high serum lipid levels

Ratio <.8mg/g is abnormal Premature infants with hemolysis due

to vit e def.have elevated platelet counts

Ref:nelson vol 1 .18 th ed ,chp 49 pg263.

Treatment of vit e def

In neonates dose 25-50 units/day for 1week

TOXICITY NO TOXIC EFFECT HAS BEEN

REPORTED .

Health hopes of Vit E

Heart Disease: Mixed results

Cancer: Promising but not conclusive› Breast cancer: two opposing studies› Colon and G.I. cancer: probably no benefit› Prostate and bladder cancer: possible

benefit

Alzheimer’s: theoretical but not well studied

STUDY SHOWS

1998: “Antioxidant vitamins and nuclear opacities: the longitudinal study of cataract”Cataract risk reduced by ½ in Vit E supplement users

764 participant observational study (low significance)