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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.
.
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)