Mitochondrial Redox Dysfunction and Environmental Exposures

Samuel W. Caito, Michael Aschner

Research output: Contribution to journalArticle

37 Scopus citations

Abstract

Significance: 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. Recent Advances: New interest is emerging not only into the roles of mitochondria in disease development and progression but also as a target for environmental toxicants. Critical Issues: 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. Future Directions: 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.

Original languageEnglish (US)
Pages (from-to)578-595
Number of pages18
JournalAntioxidants and Redox Signaling
Volume23
Issue number6
DOIs
Publication statusPublished - Aug 20 2015

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ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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