内毒素中毒小鼠脂质过氧化的证据。
Evidence for lipid peroxidation in endotoxin-poisoned mice.
作者信息
Peavy D L, Fairchild E J
出版信息
Infect Immun. 1986 May;52(2):613-6. doi: 10.1128/iai.52.2.613-616.1986.
Abstract
Ethane has been identified and quantitated in air exhaled by mice following intraperitoneal injection of 20, 40, or 200 mg of Escherichia coli O111:B4 lipopolysaccharide (LPS) per kg. Significant increases in ethane concentration occurred within 1 to 5 h after LPS administration. In addition, increased concentrations of malondialdehyde were found in crude homogenates of livers obtained from mice 16 h after administration of 20 mg of LPS per kg. These results suggest that lipid peroxidation may be an important mechanism responsible for LPS toxicity.
摘要
在给小鼠腹腔注射每千克20、40或200毫克大肠杆菌O111:B4脂多糖（LPS）后，已在小鼠呼出的空气中鉴定并定量了乙烷。LPS给药后1至5小时内，乙烷浓度显著增加。此外，在给每千克体重20毫克LPS的小鼠给药16小时后，从其肝脏的粗匀浆中发现丙二醛浓度升高。这些结果表明，脂质过氧化可能是LPS毒性的一个重要机制。
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