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植物线粒体电子传递的变化会改变细胞内活性氧的水平以及对细胞死亡信号分子的敏感性。

Changes in plant mitochondrial electron transport alter cellular levels of reactive oxygen species and susceptibility to cell death signaling molecules.

作者信息

Amirsadeghi Sasan, Robson Christine A, McDonald Allison E, Vanlerberghe Greg C

机构信息

Department of Life Sciences, University of Toronto Scarborough, 1265 Military Trail, Toronto, ON, Canada M1C1A4.

出版信息

Plant Cell Physiol. 2006 Nov;47(11):1509-19. doi: 10.1093/pcp/pcl016. Epub 2006 Sep 30.

DOI:10.1093/pcp/pcl016
PMID:17012741
Abstract

Transgenic tobacco (Nicotiana tabacum) lacking mitochondrial alternative oxidase (AOX) have been compared with wild-type (Wt) tobacco using two different systems, either suspension cell cultures or leaves. In both systems, a lack of AOX was accompanied by an increase in some anti-oxidant defenses, consistent with the hypothesis that a lack of AOX increases the mitochondrial generation of reactive oxygen species (ROS). In most cases, this increase in anti-oxidant defenses could more than offset the presumed increased rate of ROS generation, resulting paradoxically in a lower steady-state level of ROS than was found in Wt leaves or suspension cells. We also found that the amount of cell death induced by salicylic acid or nitric oxide correlated strongly with the level of ROS (irrespective of the level of AOX), while death induced by azide was dependent upon the presence or absence of AOX. These results suggest that susceptibility to cell death by signaling molecules (salicylic acid and nitric oxide) is dependent upon the steady-state cellular level of ROS and that AOX levels clearly contribute to this steady state, perhaps by influencing the rate of mitochondrial-generated ROS and hence the cellular level of anti-oxidant defenses.

摘要

已使用悬浮细胞培养或叶片这两种不同系统,将缺乏线粒体交替氧化酶(AOX)的转基因烟草(烟草)与野生型(Wt)烟草进行了比较。在这两种系统中,AOX的缺乏都伴随着一些抗氧化防御的增加,这与缺乏AOX会增加线粒体活性氧(ROS)生成的假设一致。在大多数情况下,这种抗氧化防御的增加可以超过假定的ROS生成速率的增加,矛盾的是,导致ROS的稳态水平低于Wt叶片或悬浮细胞中的水平。我们还发现,水杨酸或一氧化氮诱导的细胞死亡量与ROS水平密切相关(与AOX水平无关),而叠氮化物诱导的死亡则取决于AOX的存在与否。这些结果表明,信号分子(水杨酸和一氧化氮)对细胞死亡的易感性取决于ROS的细胞稳态水平,并且AOX水平显然有助于这种稳态,可能是通过影响线粒体产生ROS的速率,从而影响细胞抗氧化防御的水平。

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