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四氯化碳对离体大鼠肝细胞中磷脂酶A2的激活作用。

Activation of phospholipase A2 by carbon tetrachloride in isolated rat hepatocytes.

作者信息

Glende E A, Pushpendran C K

出版信息

Biochem Pharmacol. 1986 Oct 1;35(19):3301-7. doi: 10.1016/0006-2952(86)90427-2.

DOI:10.1016/0006-2952(86)90427-2
PMID:3094537
Abstract

Freshly isolated rat hepatocytes were exposed to carbon tetrachloride (CCl4) for periods up to 4 hr. Phospholipase A2 activity of these preparations was determined by measuring either the release of [3H]arachidonic acid from cellular phospholipids prelabeled with [3H]arachidonic acid or by measuring the formation of [14C]lysophosphatidylethanolamine from cellular lipids prelabeled with [14C]ethanolamine. Through the use of hexane-partition extraction and thin-layer chromatographic analysis of hepatocyte lipid extracts it was found that CCl4 stimulated phospholipase A2 activity in a dose- and time-dependent manner. Carbon tetrachloride at concentrations of 0.23 to 1.3 mM produced a 1.4- to 5.3-fold increase in phospholipase activity which was initiated within 30-60 min of incubation at 37 degrees. The role of phospholipase activation as a secondary mechanism of CCl4-induced hepatocyte injury is discussed.

摘要

将新鲜分离的大鼠肝细胞暴露于四氯化碳(CCl4)中长达4小时。通过测量从预先用[3H]花生四烯酸标记的细胞磷脂中释放的[3H]花生四烯酸,或通过测量从预先用[14C]乙醇胺标记的细胞脂质中形成的[14C]溶血磷脂酰乙醇胺,来测定这些制剂的磷脂酶A2活性。通过对肝细胞脂质提取物进行己烷分配萃取和薄层色谱分析,发现CCl4以剂量和时间依赖性方式刺激磷脂酶A2活性。浓度为0.23至1.3 mM的四氯化碳使磷脂酶活性增加了1.4至5.3倍,这种增加在37℃孵育30至60分钟内开始。讨论了磷脂酶激活作为CCl4诱导的肝细胞损伤的次要机制的作用。

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引用本文的文献

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Inhibitory effects of inhibitors of arachidonic acid metabolism on the evolution of rat liver preneoplastic foci into nodules and hepatocellular carcinomas with or without phenobarbital exposure.花生四烯酸代谢抑制剂对大鼠肝脏癌前病灶演变为结节及肝细胞癌的抑制作用,有无苯巴比妥暴露情况均涉及。
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Late preventive effects of quinacrine on carbon tetrachloride induced liver necrosis.
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