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小鼠氰化物中毒后脑脂质的过氧化作用。

Peroxidation of brain lipids following cyanide intoxication in mice.

作者信息

Johnson J D, Conroy W G, Burris K D, Isom G E

机构信息

Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, IN 47907.

出版信息

Toxicology. 1987 Oct 12;46(1):21-8. doi: 10.1016/0300-483x(87)90134-x.

Abstract

Lipid peroxidation of brain lipids as determined by the conjugated diene method was observed in mice following administration of sublethal doses of potassium cyanide (KCN). Conjugated diene production was dose- and time-dependent; 10 mg/kg KCN produced detectable levels of conjugated dienes at 30 min post cyanide, whereas, 15 mg/kg produced marked levels of conjugated dienes over a 10-60-min period after KCN. Pretreatment of mice with either diltiazem (600 micrograms/kg, i.v.) or allopurinol (25 mg/kg, i.v.) blocked the generation of conjugated dienes. These results suggest lipid peroxidation of neuronal membranes play a role in cyanide intoxication and this action is related to altered regulation of neuronal calcium homeostasis and activation of xanthine oxidase.

摘要

用共轭二烯法测定脑脂质的脂质过氧化反应,在给小鼠注射亚致死剂量的氰化钾(KCN)后被观察到。共轭二烯的产生呈剂量和时间依赖性;10mg/kg的KCN在氰化物给药后30分钟产生可检测水平的共轭二烯,而15mg/kg在KCN给药后的10 - 60分钟内产生显著水平的共轭二烯。用硫氮䓬酮(600微克/千克,静脉注射)或别嘌呤醇(25毫克/千克,静脉注射)预处理小鼠可阻断共轭二烯的生成。这些结果表明神经元膜的脂质过氧化反应在氰化物中毒中起作用,并且这种作用与神经元钙稳态调节改变和黄嘌呤氧化酶激活有关。

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