Abstract
The pathological states observed in vitamin E deficiencies have been suggested to result from the action of lipid peroxides on sulfhydryl-sensitive enzyme systems. Vitamin E antagonists, such as unsaturated fat, o-cresyl esters, carbon tetrachloride, pyridine, sulfathiazole, sulfaguanidine, and sodium sulfite, may act as pro-oxidants. They promote the production of lipid peroxides in the body tissues, and thus increase the need for vitamin E.