Vitamin E protection against in vivo lipid peroxidation initiated in rats by methyl ethyl ketone peroxide as monitored by pentane

Abstract

Vitamin E, selenium, vitamin C, and methionine were administered to rats in various combinations by diet and ip injections (12 treatment groups) in order to rank the individual and combined protective ability of the biological antioxidants at minimum daily requirement levels and at pharmacological levels against lipid peroxidation initiated by 50 mg methyl ethyl ketone peroxide (MEKP)/kg body wt. In vivo lipid peroxidation was monitored throughout a 3-hr period by measuring pentane expired in the breath. Rats fed 30 IU dl-α-tocopherol acetate/kg diet significantly ( p < 0.001) decreased pentane production at 20 min by 88% compared to rats fed a vitamin E- and selenium-deficient diet. Rats given five ip injections of 180 IU dl-α-tocopherol acetate/kg body wt further reduced expired pentane by 83% ( p < 0.001) beyond the protection afforded by dietary vitamin E. Neither additive nor synergistic protection was found when other antioxidants were given in combination with vitamin E. Vitamin E was the primary protective antioxidant. Pentane expired by individual rats from the various treatment groups strongly correlated ( r = 0.92, p < 0.001) with the plasma vitamin E status. Plasma vitamin E above the level of 0.5 mg total tocopherol/g total lipid prevented substantial increases in pentane production and blood hemolysis brought on by MEKP. A pharmacological dose of 175 mg vitamin C/kg body wt given on 3 consecutive days to vitamin E- and selenium-deficient rats potentiated MEKP toxicity. The vitamin C pretreatment caused a doubling of pentane levels and mortality within 3 hr.