Vitamin E does not have a precisely defined metabolic function
المؤلف:
Peter J. Kennelly, Kathleen M. Botham, Owen P. McGuinness, Victor W. Rodwell, P. Anthony Weil
المصدر:
Harpers Illustrated Biochemistry
الجزء والصفحة:
32nd edition.p540
2025-12-15
46
No unequivocal unique function for vitamin E has been defined. It acts as a lipid-soluble antioxidant in cell mem branes, where many of its functions can be provided by synthetic antioxidants, and is important in maintaining the fluidity of cell membranes. It also has a (relatively poorly defined) role in cell signaling. Vitamin E is the generic descriptor for two families of compounds, the tocopherols and the tocotrienols (Figure 1). The different vitamers have different biologic potency; the most active is d-α-tocopherol, and it is usual to express vitamin E intake in terms of milligrams d-α-tocopherol equivalents. Synthetic dl-α-tocopherol does not have the same biologic potency as the naturally occurring compound.
Fig1. Vitamin E vitamers.In α-tocopherol and tocotrienol R1 , R2 , and R3 are all –CH3 groups. In the β-vitamers R2 is H, in the γ-vitamers R1 is H, and in the δ-vitamers R1 and R2 are both H.
Vitamin E Is the Major Lipid-Soluble Antioxidant in Cell Membranes & Plasma Lipoproteins
The main function of vitamin E is as a chain-breaking, free radical–trapping antioxidant in cell membranes and plasma lipoproteins by reacting with the lipid peroxide radicals formed by peroxidation of polyunsaturated fatty acids. The tocopheroxyl radical is relatively unreactive, and ultimately forms nonradical compounds. Commonly, the tocopheroxyl radical is reduced back to tocopherol by reaction with vitamin C from plasma. The resultant, stable, monodehydroascorbate radical then undergoes enzymic or nonenzymic reaction to yield ascorbate and dehydroascorbate, neither of which is a radical.
Vitamin E Deficiency
In experimental animals, vitamin E deficiency results in resorption of fetuses and testicular atrophy. Dietary deficiency of vitamin E in human beings is unknown, although patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic liver disease suffer deficiency because they are unable to absorb or transport the vitamin, leading to nerve and muscle membrane damage. Premature infants are born with inadequate reserves of the vitamin. The erythrocyte membranes are abnormally fragile as a result of lipid peroxidation, leading to hemolytic anemia.
الاكثر قراءة في الكيمياء الحيوية
اخر الاخبار
اخبار العتبة العباسية المقدسة
