Abstract
A variety of diseases have been associated with excessive reactive oxygen species (ROS), which are produced mostly in the mitochondria as byproducts of normal cell respiration. The interrelationship between ROS and mitochondria suggests shared pathogenic mechanisms in mitochondrial and ROS-related diseases. Defects in oxidative phosphorylation can increase ROS production, whereas ROS-mediated damage to biomolecules can have direct effects on the components of the electron transport system. Here, we review the molecular mechanisms of ROS production and damage, as well as the existing evidence of mitochondrial ROS involvement in human diseases.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 449-457 |
| Number of pages | 9 |
| Journal | Seminars in Cell and Developmental Biology |
| Volume | 12 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jan 1 2001 |
Keywords
- Aging
- Mitochondria
- mtDNA diseases
- Neurodegeneration
- Reactive oxygen species
ASJC Scopus subject areas
- Developmental Biology
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Cite this
Kirkinezos, I. G., & Moraes, C. T. (2001). Reactive oxygen species and mitochondrial diseases. Seminars in Cell and Developmental Biology, 12(6), 449-457. https://doi.org/10.1006/scdb.2001.0282