Mitochondria targeting by environmental stressors: Implications for redox cellular signaling.

Mitochondria targeting by environmental stressors: Implications for redox cellular signaling.
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DOI:
10.1016/j.tox.2017.07.013
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发表时间:
2017-11-01
期刊:
影响因子:
4.5
通讯作者:
Bonini MG
Bonini MG
中科院分区:
医学3区
文献类型:
--
作者:
Blajszczak C;Bonini MG

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线粒体是细胞的动力源,也是代谢和信号中心,调节从基本生理到表型决定命运的各种细胞功能。人们普遍认为,线粒体中产生的活性氧物种(ROS)参与了细胞信号的调节,并且存在着在高ROS基线下工作的线粒体。然而,线粒体如何适应持续的高ROS状态以及扰乱氧化还原平衡的环境应激源并不完全清楚。在这里,我们将回顾一些目前的概念,关于线粒体如何抵抗氧化损伤,当氧化损伤过度到损害功能的程度时,它们如何被取代,以及一些环境毒物(即重金属)对线粒体ROS(MtROS)产生的调节有什么影响,这与它们对细胞和组织的毒性作用有关。
Mitochondria are cellular powerhouses as well as metabolic and signaling hubs, regulating diverse cellular functions from basic physiology to phenotypic fate determination. It is widely accepted that reactive oxygen species (ROS) generated in mitochondria participate in the regulation of cellular signaling and that there are mitochondria which operate at a high ROS baseline. However, how mitochondria adapt to persistently high ROS states as well as to environmental stressors that disturb the redox balance is not completely understood. Here we will review some of the current concepts regarding how mitochondria resist oxidative damage, how they are replaced when oxidative damage is excessive to an extent that compromises function, and what is the effect of some environmental toxicants (i.e. heavy metals) on the regulation of mitochondrial ROS (mtROS) production which are linked to their toxic effects on cells and tissues.
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