Antioxidant relationship between selenium-dependent glutathione peroxidase and tocopherol.
Glutathione peroxidase, a selenium-dependent enzyme, and tocopherol interact and may, indeed, compensate for deficiencies of one or the other. Iron-supplemented, "tocopherol-sufficient," low-birth-weight premature infants fed (selenium-poor) formulas rich in polyunsaturated fatty acid (greater than 35% of fat as PUFA) develop severe hemolysis secondary to erythrocyte phosphatidyl ethanolamine loss. By further increasing tocopherol supplementation one can prevent the clinical expression of a relative tocopherol and an absolute selenium--glutathione peroxidase deficiency. Selenium-poor cow's milk preparations containing 12--15% of fat as polyunsaturated fatty acids, trace amounts of iron, and 12--15 mg/liter of tocopherol are sufficient to maintain proper nutrition without risk of increased peroxidation.
D000818:Animals; D000975:Antioxidants / Q000097:blood; D002417:Cattle; D004912:Erythrocytes / Q000201:enzymology; D005979:Glutathione Peroxidase / Q000097:blood*; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008892:Milk / Q000378:metabolism / Q000502:physiology; D010544:Peroxidases / Q000097:blood*; D012643:Selenium / Q000502:physiology*; D014810:Vitamin E / Q000097:blood*; D014811:Vitamin E Deficiency / Q000097:blood
D000975:Antioxidants; D006454:Hemoglobins; D014810:Vitamin E; D010544:Peroxidases; D005979:Glutathione Peroxidase; D012643:Selenium