4.7 Article

Mitochondria targeting by environmental stressors: Implications for redox cellular signaling

Journal

TOXICOLOGY
Volume 391, Issue -, Pages 84-89

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.tox.2017.07.013

Keywords

Mitochondria; ROS; Redox signaling; Arsenic; Heavy metals

Funding

  1. U.S. Department of Defense Army Research Office [W911NF-15-1-0410]
  2. National Institutes of Health [1RO1HL125356, 1RO1AI131267]

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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 some mitochondria chronically operate at a high ROS baseline. However, it is not completely understood how mitochondria adapt to persistently high ROS states and to environmental stressors that disturb the redox balance. Here we will review some of the current concepts regarding how mitochondria resist oxidative damage, how they are replaced when excessive oxidative damage compromises function, and the effect of environmental toxicants (i.e. heavy metals) on the regulation of mitochondrial ROS (mtROS) production and subsequent impact.

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