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暴露于氧化应激的肝细胞中内源性核酸内切酶活性的刺激。

Stimulation of endogenous endonuclease activity in hepatocytes exposed to oxidative stress.

作者信息

McConkey D J, Hartzell P, Nicotera P, Wyllie A H, Orrenius S

机构信息

Department of Toxicology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Toxicol Lett. 1988 Aug;42(2):123-30. doi: 10.1016/0378-4274(88)90069-0.

DOI:10.1016/0378-4274(88)90069-0
PMID:2841775
Abstract

Incubation of freshly isolated rat hepatocytes with moderately toxic concentrations of menadione [2-methyl-1,4-naphthoquinone) resulted in chromatin condensation and progressive DNA fragmentation, suggestive of the stimulation of an endogenous endonuclease activity previously found to be involved in programmed cell death (apoptosis). Endonuclease activation followed upon a sustained increase in cytosolic Ca2+ concentration and preceded cell killing by 1-2 h. It is concluded that generation of oxidative stress in hepatocytes can activate processes similar to those observed during programmed cell death.

摘要

将新鲜分离的大鼠肝细胞与中等毒性浓度的甲萘醌(2-甲基-1,4-萘醌)一起孵育,导致染色质凝聚和渐进性DNA片段化,这表明先前发现参与程序性细胞死亡(凋亡)的内源性核酸内切酶活性受到刺激。核酸内切酶的激活是在细胞质Ca2+浓度持续增加之后发生的,并且在细胞死亡前1-2小时出现。结论是,肝细胞中氧化应激的产生可以激活类似于程序性细胞死亡过程中观察到的那些过程。

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Stimulation of endogenous endonuclease activity in hepatocytes exposed to oxidative stress.暴露于氧化应激的肝细胞中内源性核酸内切酶活性的刺激。
Toxicol Lett. 1988 Aug;42(2):123-30. doi: 10.1016/0378-4274(88)90069-0.
2
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