Brain alterations induced by vitamin E deficiency and intoxication with methyl ethyl ketone peroxide

Rats fed a vitamin E-deficient diet from age 3-10 weeks were either maintained on a vitamin E-deficient diet or fed a vitamin E-enriched diet for 8 subsequent weeks. The content of vitamin E, endoperoxide-derived malonaldehyde, lipofluorescent material and polyunsaturated fatty acids, and the activities of catalase, glutathione reductase, and glutathione peroxidase were then measured in cerebral tissues, with or without intoxication with methyl ethyl ketone peroxide (MEKP). For this purpose, one half of the animals in each vitamin E group received an ip injection of 5 mg MEKP per kg of body weight, which was followed 44 hours later, i.e., 4 hours before sample collection, by a second ip injection of 15 mg MEKP per kg of body weight. Despite the fact that the vitamin E concentration was 12-times lower in the brain of vitamin E-deficient rats, no significant change in other cerebral parameters was found between the two groups of animals. In contrast, the activity of selenium-glutathione peroxidase was markedly decreased in the liver of 10-week old vitamin E-deficient rats. Unexpectedly, acute systemic intoxication with MEKP caused only a small, albeit significant, decrease in glutathione reductase activity in the brain of vitamin E-sufficient rats, while no significant change in other cerebral parameters was observed in either group of animals. These results suggest that the central nervous system (CNS) is still substantially protected when its vitamin E content has been decreased to 3 micrograms/g fresh weight, and that systemic intoxication with MEKP may not cause lipid peroxidation in the CNS.