Mitochondria targeting by environmental stressors: Implications for redox cellular signaling

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 si...

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Bibliographic Details
Published in:Toxicology (Amsterdam) 2017-11, Vol.391, p.84-89
Main Authors: Blajszczak, Chuck, Bonini, Marcelo G.
Format: Article
Language:English
Subjects:
Animals
Arsenic
DNA Damage
DNA, Mitochondrial - genetics
DNA, Mitochondrial - metabolism
Ecotoxicology - methods
Environmental Exposure - adverse effects
Environmental Pollutants - toxicity
Heavy metals
Humans
Metals, Heavy - toxicity
Mitochondria
Mitochondria - drug effects
Mitochondria - genetics
Mitochondria - metabolism
Mitochondria - pathology
Oxidation-Reduction
Oxidative Stress - drug effects
Reactive Oxygen Species - metabolism
Redox signaling
ROS
Signal Transduction - drug effects
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Summary: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.
ISSN:0300-483X
1879-3185
DOI:10.1016/j.tox.2017.07.013