Vitamin E and autoxidation.
Vitamin E refers to a family of fat-soluble phenolic compounds called tocopherols, which have been established as essential nutrients in vertebrates. In animals the deficiency state has resulted in diminished reproductive capabilities, muscular dystrophy, exudative diathesis, megaloblastosis, gastrointestinal and pulmonary degeneration, and nephrosis. In humans with low vitamin E levels a subclinical diminished erythrocyte life-span has been demonstrated by hydrogen peroxide hemolysis test. This effect may have clinical significance among premature infants. The metabolic function of vitamin E appears to be as a scavenger of lipid peroxides and free oxygen radicals which enter into chain reactions to cause breakdown of lipids. Normal levels of the vitamin serve to prevent this cellular oxidative breakdown. Laboratory measurement of vitamin E is chromatographic, with HPLC presently used in both research and clinical applications. The association between vitamin E levels and hemolytic anemia in humans is currently under investigation.
D000743:Anemia, Hemolytic / Q000209:etiology; D000818:Animals; D055598:Chemical Phenomena; D002621:Chemistry; D004905:Erythrocyte Aging; D005260:Female; D005609:Free Radicals; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000209:etiology; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D009747:Nutritional Physiological Phenomena; D010084:Oxidation-Reduction; D014810:Vitamin E / Q000032:analysis / Q000378:metabolism*; D014811:Vitamin E Deficiency / Q000150:complications
D005609:Free Radicals; D008054:Lipid Peroxides; D014810:Vitamin E; D005979:Glutathione Peroxidase