Mitochondria: omega-3 in the route of mitochondrial reactive oxygen species

Int J Biochem Cell Biol. 2012 Sep;44(9):1569-73. doi: 10.1016/j.biocel.2012.06.003. Epub 2012 Jun 15.


Mitochondria are the main organelles that produce reactive oxygen species (ROS). Overproduction of ROS induces oxidative damage to macromolecules, including lipids, and can damage cellular membrane structure and functions. Mitochondria, the main target of ROS-induced damage, are equipped with a network of antioxidants that control ROS production. Dietary intake of omega-3 polyunsaturated fatty acids (ω3PUFAs) and consequently the increase in ω3PUFA content of membrane lipids may be disadvantageous to the health because ROS-induced oxidative peroxidation of ω3PUFAs within membrane phospholipids can lead to the formation of toxic products. Mitochondrial control of lipid peroxidation is one of the mechanisms that protect cell against oxidative damage. This review discusses the role of mitochondria in ROS generation and the mechanisms by which it regulates ROS production. The susceptibility to peroxidation of PUFAs by ROS raises the question of the adverse effects of ω3PUFA dietary supplementation on embryonic development and prenatal developmental outcomes.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Fatty Acids, Omega-3 / adverse effects
  • Fatty Acids, Omega-3 / pharmacology*
  • Humans
  • Mitochondria / drug effects*
  • Mitochondria / metabolism*
  • Mitochondria / pathology
  • Reactive Oxygen Species / metabolism*


  • Fatty Acids, Omega-3
  • Reactive Oxygen Species