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硝酸铅对四氯化碳肝毒性的保护作用。

Protection by lead nitrate against carbon tetrachloride hepatotoxicity.

作者信息

Pani P, Corongiu F P, Sanna A, Congiu L

出版信息

Drug Metab Dispos. 1975 May-Jun;3(3):148-54.

PMID:238813
Abstract

Pretreatment with lead nitrate of rats intoxicated with CCl4 exerted a significant protective effect against several damaging effects of the haloalkane. Liver microsomal lipid peroxidation, one of the earliest phenomena in CCl4 intoxication, was clearly inhibited by pretreating the rats with lead. The heavy metal also ameliorated the polyribosomal disaggregation caused by CCl4. Fatty infiltration in the liver, measured by the triglyceride content in the organ, was less pronounced in CCl4-poisoned rats pretreated with lead than in animals treated with the haloalkane alone. Lipid metabolism was also studied by means of Triton WR 1339-induced hypertriglyceridemia to examine the state of triglyceride secretion from liver into plasma; the higher level of plasma triglyceride in the lead-pretreated rats further strengthened the results obtained on the secretion experiments. Finally, CCl4-induced liver necrosis, as measured by serum transaminases and histological examination, was partially prevented by lead. The mechanism by which lead, an inhibitor of the drug-metabolizing enzyme system, interferes with CCl4 intoxication, is disccused.

摘要

用硝酸铅对四氯化碳中毒的大鼠进行预处理,对卤代烷的几种损伤作用具有显著的保护作用。肝微粒体脂质过氧化是四氯化碳中毒最早出现的现象之一,用铅预处理大鼠可明显抑制这一现象。这种重金属还改善了由四氯化碳引起的多核糖体解聚。通过测量肝脏中甘油三酯含量来衡量的肝脏脂肪浸润,在用铅预处理的四氯化碳中毒大鼠中比仅用卤代烷处理的动物中不那么明显。还通过Triton WR 1339诱导的高甘油三酯血症研究脂质代谢,以检查肝脏向血浆中甘油三酯分泌的状态;铅预处理大鼠中较高水平的血浆甘油三酯进一步加强了在分泌实验中获得的结果。最后,通过血清转氨酶和组织学检查测量的四氯化碳诱导的肝坏死,部分被铅预防。文中讨论了作为药物代谢酶系统抑制剂的铅干扰四氯化碳中毒的机制。

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