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在酵母中,缺失效应物半胱天冬酶和/或细胞色素 c 会导致活性氧(ROS)非依赖性、乙酸诱导的程序性细胞死亡途径的激活。

Knock-out of metacaspase and/or cytochrome c results in the activation of a ROS-independent acetic acid-induced programmed cell death pathway in yeast.

机构信息

CNR, Istituto di Biomembrane e Bioenergetica, Via Amendola 165/A, 70126 Bari, Italy.

出版信息

FEBS Lett. 2010 Aug 20;584(16):3655-60. doi: 10.1016/j.febslet.2010.07.044. Epub 2010 Aug 3.

DOI:10.1016/j.febslet.2010.07.044
PMID:20674572
Abstract

To gain further insight into yeast acetic acid-induced programmed cell death (AA-PCD) we analyzed the effects of the antioxidant N-acetyl-L-cysteine (NAC) on cell viability, hydrogen peroxide (H(2)O(2)) production, DNA fragmentation, cytochrome c (cyt c) release and caspase-like activation in wild type (wt) and metacaspase and/or cyt c-lacking cells. We found that NAC prevents AA-PCD in wt cells, by scavenging H(2)O(2) and by inhibiting both cyt c release and caspase-like activation. This shows the occurrence of a reactive oxygen species (ROS)-dependent AA-PCD. Contrarily no NAC dependent change in AA-PCD of mutant cells was detectable, showing that a ROS-independent AA-PCD can also occur.

摘要

为了更深入地了解酵母乙酸诱导的程序性细胞死亡(AA-PCD),我们分析了抗氧化剂 N-乙酰-L-半胱氨酸(NAC)对野生型(wt)和缺少介体型半胱天冬酶和/或细胞色素 c(cyt c)细胞的细胞活力、过氧化氢(H 2 O 2 )产生、DNA 片段化、细胞色素 c(cyt c)释放和半胱天冬酶样激活的影响。我们发现 NAC 通过清除 H 2 O 2 和抑制 cyt c 释放和半胱天冬酶样激活来防止 wt 细胞中的 AA-PCD。这表明发生了活性氧(ROS)依赖性的 AA-PCD。相反,在突变细胞的 AA-PCD 中未检测到 NAC 依赖性变化,表明也可能发生 ROS 非依赖性的 AA-PCD。

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