Abstract
Abstract Incubation of adrenal homogenates of tocopherol-deficient rats was shown to produce a compound which was identified as malonaldehyde. This product formed a pink color with thiobarbituric acid (TBA) which had the same absorption characteristics as authentic malonaldehyde-TBA complex. The malonaldehyde production in vitro as an index of lipid peroxidation, as tested by the TBA test, has been evaluated and compared in the various tissue homogenates of tocopherol-deficient and control rats. Lipid peroxidation in the liver homogenates of tocopherol-deficient rats reached a maximum level in 1 week. In contrast, the adrenal homogenates exhibited a progressive increase in lipid peroxidation in vitro from the 2nd to 7th week of tocopherol deprivation. The kinetic studies of lipid peroxidation reaction of adrenal homogenate during various stages of vitamin E deprivation indicated presence of a lag period in the early period of tocopherol deprivation which disappeared by 9th week of tocopherol deprivation. The extent of adrenal lipid peroxidation in vitro was about 10 times higher than in any other tissue tested. Diminution of adrenal ascorbate in the deficient group by stress, dialysis of the homogenate, or addition of ascorbic acid oxidase to the homogenate reduced lipid peroxidation in vitro. Malonaldehyde was not produced by either the particulate nor the supernatant fraction of the adrenal homogenate, but optimal amounts were formed by combining these two fractions. The ability of the supernantant fraction to catalyze formation of malonaldehyde (in the presence of adrenal particulate fraction) could be mimicked by ascorbic acid; this catalytic effect was abolished by addition of ascorbic acid oxidase. The content of adrenal ascorbate and percentage of individual fatty acids were similar in the two dietary groups at various stages of vitamin E deprivation. It is suggested that with gradual diminution of tocopherol, the high level of polyunsaturated lipids in the adrenal particulate matter, in the presence of high ascorbic acid in the adrenal supernatant solution, may contribute to the high lipid peroxidation in vitro in vitamin E-deficient rats.
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