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Vitamin EINCLUDEPICTURE "I:\\Biochemisy_2003 (G)\\dll\\alphatocopherol.jpg" \* MERGEFORMATINET Tocopherol
Vitamin E is a mixture of several related compounds known as tocopherols. Eight naturally occurring tocopherol molecules, the alpha-tocopherol molecule is the most potent of the tocopherols.
Distribution of vitamin E:
Vegetable oils are rich sources of vitamin E where as liver and eggs contain moderate amounts. Vit.E is destroyed by commercial cooking and food processing including deep freezing.
Metabolism of vitamin E:
Vitamin E is absorbed from the intestines packaged in chylomicrons. It is delivered to the tissues via chylomicron transport and then to the liver through chylomicron remnant uptake. The liver can export vitamin E in VLDLs. Due to its lipophilic nature, vitamin E accumulates in cellular membranes, fat deposits and other circulating lipoproteins. The major site of vitamin E storage is in adipose tissue.
Function of vitamin E:
The major function of vitamin E is to act as a natural antioxidant by scavenging free radicals and molecular oxygen. In particular vitamin E is important for preventing peroxidation of polyunsaturated membrane fatty acids. The vitamins E and C are interrelated in their antioxidant capabilities. Active alpha-tocopherol can be regenerated by interaction with vitamin C following scavenge of a peroxy free radical. Alternatively, alpha-tocopherol can scavenge two peroxy free radicals and then be conjugated to glucuronate for excretion in the bile.
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HYPERLINK "file:///I:\\Biochemisy_2003%20(G)\\dll\\vitamins.html" \l "top" Clinical significances of Vitamin E DeficiencyNo major disease states have been found to be associated with vitamin E deficiency due to adequate levels. Since vitamin E is absorbed from the intestines in chylomicrons, any fat malabsorption diseases can lead to deficiencies in vitamin E intake also prolonged parenteral nutrition can lead to deficiencies in vitamin E can lead to deficiencies in vitamin E .
Vitamin K
The K vitamins exist naturally as K1 (phylloquinone) in green vegetables and K2 (menaquinone) produced by intestinal bacteria and K3 is synthetic menadione.INCLUDEPICTURE "I:\\Biochemisy_2003 (G)\\dll\\vitamink1.jpg" \* MERGEFORMATINET INCLUDEPICTURE "I:\\Biochemisy_2003 (G)\\dll\\vitamink2.jpg" \* MERGEFORMATINET INCLUDEPICTURE "I:\\Biochemisy_2003 (G)\\dll\\vitamink3.jpg" \* MERGEFORMATINET Vitamin K1Vitamin K2 "n" can be 6, 7 or 9 isoprenoid groupsVitamin K3
Significant sources
Bacterial synthesis in the digestive tract
Liver
Leafy green vegetables, cabbage-type vegetables
Milk
Vitamin K-Dependent Modifications
HYPERLINK "file:///F:\\Biochemisy_2003%20(G)\\dll\\vitamins.html" \l "k" Vitamin K is a cofactor in the carboxylation of glutamine residues that present in blood clotting factors. The result of this type of reaction is a gama-carboxyglutamate (called a gla residue).
INCLUDEPICTURE "F:\\Biochemisy_2003 (G)\\dll\\glaresidue.gif" \* MERGEFORMATINET
Structure of a gla residue
The formation of gla residues within several proteins of the HYPERLINK "file:///F:\\Biochemisy_2003%20(G)\\dll\\blood-coagulation.html" blood clotting cascade is critical for their normal function. The presence of gla residues allows the protein to chelate calcium ions and thereby render an altered conformation and biological activity to the protein.
Function of vitamin K:
1. formation of gama carboxyglutamate(gla): The major function of the K vitamins is in the maintenance of normal levels of the HYPERLINK "file:///I:\\Biochemisy_2003%20(G)\\dll\\blood-coagulation.html" blood clotting proteins, factors II, VII, IX, X , which are synthesized in the liver as inactive precursor proteins. Conversion from inactive to active clotting factor requires vitamin K-dependent carboxylation of glutamic acid residues. This forms a mature clotting factor that contains modified glutamate residues which are gama-carboxyglutamate (gla). This process is most clearly understood for factor II, also called preprothrombin. Prothrombin is modified preprothrombin.
2. interaction of prothrombin with platlets: The gla residues are effective calcium ion chelators. Upon chelation of calcium, prothrombin interacts with phospholipids in membranes and is proteolysed to thrombin through the action of activated factor X (Xa).
3.Role of gla residues in other protein: Gla also present in osteocalcin of bone, and in protein involved in the degradation of blood clot.
METABOLIC REACTION OF VITAMIN K
SHAPE \* MERGEFORMATAs a cofactor to the carboxylase that generates gamma-carboxyglutamic acid, Vitamin K undergoes a cycle of oxidation and reduction that allows its reuse
Vitamin K is reduced to Vitamin KH2
Oxygenation of vitamin KH2 provides the energy to drive the carboxylation reaction, leading to formation of gamma-carboxyglutamic acid residues and Vitamin K oxide
Vitamin K oxide is reduced by another reductase back to Vitamin K, ready to enter another cycle. Anticoagulants block the reduction of Vitamin K oxide to Vitamin K, explaining their antagonistic effects on this cycle
Clinical significance of Vitamin K Deficiency
Naturally occurring vitamin K is absorbed from the intestines only in the presence of bile salts and other lipids through interaction with chylomicrons. Therefore, fat malabsorptive diseases can result in vitamin K deficiency. E.g. pancreatic disease, biliary disease ,intestinal mucosal atrophy or any cause of steatorrhea.The synthetic vitamin K3 is water soluble and absorbed irrespective of the presence of intestinal lipids and bile. Since the vitamin K2 form is synthesized by intestinal bacteria, deficiency of the vitamin in adults is rare. However, long term antibiotic treatment can lead to deficiency in adults. Deficiency is accompanied by bleeding tendency with prolonged prothrombin time. If these findings are due to deficiency of the vitamin they can be corrected by parenteral administration.
Vitamin K deficiency is most often due to treatment with anticoagulants (e.g. warfarin), it lead to reduced levels of the vitamin K dependent coagulation factors and lead to haemorrhge, (so vitamin K is considered as antidote for warfarin).
In newborn, plasma concentration of the vitamin is lower than adults because:
1. The intestine of newborn infants is sterile, therefore, vitamin K deficiency in infants is possible.
2.Very little of the vitamin can be transported across the placenta.
Deficiency may be severe enough to cause hemorrhagic disease of newborn, a condition which may present within 2 to 3 days of birth.
Toxicity:
Prolong administration of large doses of vitamin K can produce hemolytic anemia and jaundice in infant, due to toxic effect on red blood cells
Summary:
Vitamin E is a mixture of several related compounds known as tocopherols
The major function of vitamin E is to act as a natural antioxidant
Active alpha-tocopherol can be regenerated by interaction with vitamin C following scavenge of a peroxy free radical
The major function of the K vitamins is in the maintenance of normal levels of the HYPERLINK "file:///I:\\Biochemisy_2003%20(G)\\dll\\blood-coagulation.html" \t "_parent" blood HYPERLINK "file:///I:\\Biochemisy_2003%20(G)\\dll\\blood-coagulation.html" \t "_parent" clotting proteins
In adults vit.K deficiency may occur in: 1.fat malabsorptive diseases... 2.after long term antibiotic treatment.
vitamin K2 form is synthesized by intestinal bacteria,
The intestine of newborn infants is sterile, therefore, vitamin K deficiency in infants is possible