Enhanced lung toxicity of O2 in selenium-deficient rats.
To test the hypothesis that glutathione (GSH) peroxidase is an important component of the lung's anti-oxidant defense systemes, O2 toxicity was studied in selenium (Se)-deficient rats. Chronic respiratory disease free rats fed a Se-deficient diet or a diet supplemented with Se for 40 days after weaning were exposed to 80% O2 at atmospheric pressures for 3 days. Activities of GSH peroxidase in lungs of Se-deficient rats were markedly lower than corresponding activities in rats supplemented with 0.5 or 2.0 ppm Se. With O2 exposure, 35% of the rats fed the Se-deficient regimen died, whereas all rats fed Se-supplemented diets survived. Lungs from surviving Se-deficient rats exposed to O2 were edematous. The data suggest that the toxic effects of O2 are enhanced in Se-deficient rats and that nutritional factors contribute to lung susceptibility to oxidant-induced damage.
D000818:Animals; D005979:Glutathione Peroxidase / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D008171:Lung Diseases / Q000139:chemically induced* / Q000201:enzymology / Q000473:pathology; D008297:Male; D009929:Organ Size / Q000187:drug effects; D010100:Oxygen / Q000009:adverse effects*; D051381:Rats; D012643:Selenium / Q000172:deficiency*; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology
D014810:Vitamin E; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D012643:Selenium; D010100:Oxygen