Under a rather rigidly defined set of empirical conditions, the kinetics of production of a specific tocopherol‐deficiency sign, creatinuria, in the rat were comparable to the kinetics of the autoxidation of pure polyunsaturated fatty acids in model systemsin vitro. The tocopherol requirement of the rat under these conditions was clearly related to the kinetics of lipid peroxidation. Dietary, biologically available selenium decreased the rate of production of creatinuria and the rate of disappearance of tissue polyunsaturated fatty acids (PUFA) equally and, therefore, may have functioned as a lipid antioxidantin vivo. A hypothetical model of lipid peroxidation was prepared in an attempt to describe the interaction of PUFA, tocopherol, biologically available selenium, and sulfur amino acids.
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