Title: Mitochondrial Redox Dysfunction and Environmental Exposures.
Authors: Caito, Samuel W; Aschner, Michael
Published In Antioxid Redox Signal, (2015 Aug 20)
Abstract: Mitochondria are structurally and biochemically diverse, even within a single type of cell. Protein complexes localized to the inner mitochondrial membrane synthesize ATP by coupling electron transport and oxidative phosphorylation. The organelles produce reactive oxygen species (ROS) from mitochondrial oxygen and ROS can, in turn, alter the function and expression of proteins used for aerobic respiration by post-translational and transcriptional regulation.New interest is emerging not only into the roles of mitochondria in disease development and progression but also as a target for environmental toxicants.Dysregulation of respiration has been linked to cell death and is a major contributor to acute neuronal trauma, peripheral diseases, as well as chronic neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease.Here, we discuss the mechanisms underlying the sensitivity of the mitochondrial respiratory complexes to redox modulation, as well as examine the effects of environmental contaminants that have well-characterized mitochondrial toxicity. The contaminants discussed in this review are some of the most prevalent and potent environmental contaminants that have been linked to neurological dysfunction, altered cellular respiration, and oxidation.
PubMed ID: 25826672
MeSH Terms: Animals; Central Nervous System Diseases/chemically induced; Central Nervous System Diseases/metabolism*; Environmental Exposure*; Environmental Pollutants/toxicity*; Humans; Mitochondria/drug effects; Mitochondria/metabolism*; Oxidation-Reduction; Oxidative Stress; Reactive Oxygen Species/metabolism