Mitochondria targeting by environmental stressors: Implications for redox cellular signaling. Toxicology 2017 Nov 01;391:84-89
Date
07/29/2017Pubmed ID
28750850Pubmed Central ID
PMC5939563DOI
10.1016/j.tox.2017.07.013Scopus ID
2-s2.0-85028334909 (requires institutional sign-in at Scopus site) 91 CitationsAbstract
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.
Author List
Blajszczak C, Bonini MGMESH terms used to index this publication - Major topics in bold
AnimalsDNA Damage
DNA, Mitochondrial
Ecotoxicology
Environmental Exposure
Environmental Pollutants
Humans
Metals, Heavy
Mitochondria
Oxidation-Reduction
Oxidative Stress
Reactive Oxygen Species
Signal Transduction
