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脂质过氧化在四氯化碳诱导的肝微粒体酶损伤中的作用:使用微粒体和分离的肝细胞进行的体外比较研究。

The role of lipid peroxidation in CCl4-induced damage to liver microsomal enzymes: comparative studies in vitro using microsomes and isolated liver cells.

作者信息

Poli G, Cheeseman K, Slater T F, Dianzani M U

出版信息

Chem Biol Interact. 1981 Oct;37(1-2):13-24. doi: 10.1016/0009-2797(81)90162-9.

Abstract

The question as to whether CCl4 decreases the activities of glucose-6-phosphatase and cytochrome P-450 in liver endoplasmic reticulum mainly through its action in stimulating lipid peroxidation has been investigated using Promethazine to block lipid peroxidation. The investigation, moreover, has compared the effects of CCl4, with and without Promethazine, on isolated rat hepatocytes with corresponding effects on rat liver microsomal suspensions. Our data give no support for the view that products of lipid peroxidation are the main cause of the decrease in cytochrome P-450 observed in CCl4-intoxication. However, our present results are consistent with lipid peroxidation being a major contributory factor to the decrease in glucose-6-phosphatase activity observed in CCl4-induced liver injury.

摘要

使用异丙嗪来阻断脂质过氧化反应,研究了四氯化碳(CCl4)是否主要通过刺激脂质过氧化作用来降低肝内质网中葡萄糖-6-磷酸酶和细胞色素P-450的活性。此外,该研究还比较了有或无异丙嗪存在时CCl4对分离的大鼠肝细胞的影响以及对大鼠肝微粒体悬浮液的相应影响。我们的数据不支持脂质过氧化产物是CCl4中毒时观察到的细胞色素P-450降低的主要原因这一观点。然而,我们目前的结果与脂质过氧化是CCl4诱导的肝损伤中观察到的葡萄糖-6-磷酸酶活性降低的主要促成因素这一观点一致。

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