Johnson J D, Conroy W G, Burris K D, Isom G E
Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, IN 47907.
Toxicology. 1987 Oct 12;46(1):21-8. doi: 10.1016/0300-483x(87)90134-x.
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.
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。