Effect of alpha-Tocopherol on endotoxicosis.
The effect of alpha-tocopherol in endotoxicosis was studied. The alpha-tocopherol level significantly decreased in mouse liver 18 hr after endotoxin administration, thereafter tending to increase to approach the normal range. In endotoxin-tolerant mouse liver, the lipid peroxide level was reduced to less than half of that in nontolerant animals following endotoxin challenge. The liver lipid peroxide level and serum lactate dehydrogenase or acid phosphatase leakage were studied in mice fed a vitamin E-deficient (ED) diet and a vitamin E-supplemented (ES) diet for 40 days. ED mouse liver exhibited a higher formation of lipid peroxide after endotoxin was given while there was a markedly lower level in ES mouse liver. There was significantly more serum lactate dehydrogenase or acid phosphatase leakage in ED mice than in ES mice after endotoxin administration. There was about a 25% decrease in liver superoxide dismutase (SOD) activity in endotoxin-poisoned mice fed both the normal and the ED diets, while the activity was at a higher level in ES-fed mice. These results suggest that alpha-tocopherol may be helpful in preventing membrane instability in endotoxin poisoning.
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D004032:Diet; D004731:Endotoxins / Q000506:poisoning*; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008297:Male; D051379:Mice; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*
D004731:Endotoxins; D007527:Isoenzymes; D008054:Lipid Peroxides; D014810:Vitamin E; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D000135:Acid Phosphatase