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缺硒大鼠中氧气增强的肺毒性。

Enhanced lung toxicity of O2 in selenium-deficient rats.

作者信息

Cross C E, Hasegawa G, Reddy K A, Omaye S T

出版信息

Res Commun Chem Pathol Pharmacol. 1977 Apr;16(4):695-706.

PMID:860085
Abstract

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.

摘要

为了验证谷胱甘肽(GSH)过氧化物酶是肺部抗氧化防御系统重要组成部分这一假说,对缺硒大鼠的氧气毒性进行了研究。断奶后喂食缺硒饲料或添加硒饲料40天的无慢性呼吸道疾病大鼠,在常压下暴露于80%氧气环境中3天。缺硒大鼠肺中谷胱甘肽过氧化物酶的活性显著低于补充0.5或2.0 ppm硒的大鼠相应的活性。暴露于氧气环境后,喂食缺硒饲料的大鼠中有35%死亡,而所有喂食补充硒饲料的大鼠存活。暴露于氧气环境的存活缺硒大鼠的肺出现水肿。数据表明,缺硒大鼠中氧气的毒性作用增强,营养因素导致肺部易受氧化诱导损伤。

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