The role of lipid peroxidation during chronic and acute exposure to ethanol as determined by pentane expiration in the rat

Abstract Weanling rats were fed one of 3 diets containing 0, 11 or 200 international units (IU) dl‐α‐tocopherol acetate/kg diet for 4 weeks. Following this period, the drinking water was replaced with an 18% solution of ethanol (v/v). An isocaloric D‐glucose solution was substituted for the drinking water of a control group of rats fed the vitamin‐E‐deficient diet for 4 weeks. The 4 treatment groups were maintained on the diet and drinking regimen for 20 weeks. Basal levels of expired pentane were determined at weeks 0, 1, 3, 5, 7 and 9. Chronic ethanol consumption did not influence basal pentane production during the 9‐week treatment. Basal levels of expired pentane were affected by dietary vitamin E. Rats supplemented with vitamin E had basal pentane levels less than one‐half of the level of rats fed a vitamin‐E‐deficient diet ( p <0.001). After 14 weeks of treatment, the 2 groups of rats fed a vitamin‐E‐deficient diet were administered p.o. an acute dose of 6 g of ethanol/kg body wt. Pentane expired above basal levels during the following 4‐hr period correlated with the amount of hepatic triglycerides determined at the conclusion of the experiment. The etiology of ethanol toxicity is a complex and multifactorial system made up to many biological variables that influence lipid peroxidation. The appropriate choices of experimental designs and methods are important in examining the role of lipid peroxidation.