Reactive oxygen species and mitochondrial diseases

Ilias G. Kirkinezos, Carlos T. Moraes

Research output: Contribution to journalArticle

263 Scopus citations

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 languageEnglish (US)
Pages (from-to)449-457
Number of pages9
JournalSeminars in Cell and Developmental Biology
Volume12
Issue number6
DOIs
StatePublished - Jan 1 2001

Keywords

  • Aging
  • Mitochondria
  • mtDNA diseases
  • Neurodegeneration
  • Reactive oxygen species

ASJC Scopus subject areas

  • Developmental Biology

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