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矛盾的是,先前获得的抗氧化活性会增强氧化应激诱导的细胞死亡。

Paradoxically, prior acquisition of antioxidant activity enhances oxidative stress-induced cell death.

作者信息

Murik Omer, Kaplan Aaron

机构信息

Department of Plant and Environmental Sciences, The Hebrew University of Jerusalem, 91904 Jerusalem, Israel.

出版信息

Environ Microbiol. 2009 Sep;11(9):2301-9. doi: 10.1111/j.1462-2920.2009.01957.x. Epub 2009 Jun 7.

DOI:10.1111/j.1462-2920.2009.01957.x
PMID:19508337
Abstract

Oxidative stress has been implicated in the induction of programmed cell death in a wide variety of organisms. Acquiring antioxidant capacity is thought to enhance the viability of cells challenged by a subsequent oxidative stress. Counter-intuitively, we show that in two phytoplankton species, Chlamydomonas reinhardtii and Peridinium gatunense, representing the green and red plastid lineages, oxidative stress induced cell death in cultures that already possessed high antioxidant activity but not in cells that exhibited low activity. Cell death of low antioxidant possessing cultures was markedly enhanced by the addition of dehydroascorbate, a product of ascorbate peroxidase (APX), but not of ascorbate or reduced glutathione, and was preceded by increased metacaspase expression and activity. These data suggested that the level of APX and its products, strongly upregulated by oxidative stress, serves as a possible surveillance signal, reporting that the cells already experienced an earlier oxidative stress. Our data presents a novel role of APX in antioxidant activity and response to oxidative stress in photosynthetic microorganisms. Elimination of cysts production by phytoplankton cells that were already damaged by oxidative stress (indicated by the rise in oxidized proteins) as the inoculum for the following year's population may be the evolutionary trigger for this phenomenon.

摘要

氧化应激与多种生物体中程序性细胞死亡的诱导有关。获得抗氧化能力被认为可以提高受到后续氧化应激挑战的细胞的活力。与直觉相反的是,我们发现,在代表绿色和红色质体谱系的两种浮游植物莱茵衣藻和加通梨甲藻中,氧化应激在已经具有高抗氧化活性的培养物中诱导细胞死亡,而在抗氧化活性低的细胞中则不会。添加抗坏血酸过氧化物酶(APX)的产物脱氢抗坏血酸可显著增强低抗氧化能力培养物的细胞死亡,但添加抗坏血酸或还原型谷胱甘肽则不会,并且在细胞死亡之前,metacaspase的表达和活性会增加。这些数据表明,APX及其产物的水平在氧化应激作用下大幅上调,可能作为一种监测信号,表明细胞已经经历了早期的氧化应激。我们的数据揭示了APX在光合微生物抗氧化活性和对氧化应激反应中的新作用。将已经受到氧化应激损伤(以氧化蛋白增加为指标)的浮游植物细胞产生的囊肿作为次年种群的接种物去除,可能是这一现象的进化触发因素。

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