There is no evidence that mitochondria are the main source of reactive oxygen species in mammalian cells
- PMID: 21303703
- DOI: 10.1016/j.mito.2011.02.001
There is no evidence that mitochondria are the main source of reactive oxygen species in mammalian cells
Abstract
It is often assumed that mitochondria are the main source of reactive oxygen species (ROS) in mammalian cells, but there is no convincing experimental evidence for this in the literature. What evidence there is suggests mitochondria are a significant source for ROS, which may have physiological and pathological effects. But quantitatively, endoplasmic reticulum and peroxisomes have a greater capacity to produce ROS than mitochondria, at least in liver. In most cells and physiological or pathological conditions there is a lack of evidence for or against mitochondria being the main source of cellular ROS. Mitochondria can rapidly degrade ROS and thus are potential sinks for ROS, but whether mitochondria act as net sources or sinks within cells in particular conditions is unknown.
Copyright © 2011 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
Similar articles
-
Endogenous mechanisms of reactive oxygen species (ROS) generation.Postepy Hig Med Dosw (Online). 2016 Nov 14;70(0):1150-1165. doi: 10.5604/17322693.1224259. Postepy Hig Med Dosw (Online). 2016. PMID: 27892899 Review.
-
Reactive oxygen species and peroxisomes: struggling for balance.Biofactors. 2009 Jul-Aug;35(4):346-55. doi: 10.1002/biof.48. Biofactors. 2009. PMID: 19459143 Review.
-
Acyl-CoA-induced generation of reactive oxygen species in mitochondrial preparations is due to the presence of peroxisomes.Free Radic Biol Med. 2009 Sep 1;47(5):503-9. doi: 10.1016/j.freeradbiomed.2009.05.006. Epub 2009 May 13. Free Radic Biol Med. 2009. PMID: 19442717
-
Intracellular generation of reactive oxygen species by mitochondria.Biochem Pharmacol. 2005 Mar 1;69(5):719-23. doi: 10.1016/j.bcp.2004.12.002. Epub 2005 Jan 20. Biochem Pharmacol. 2005. PMID: 15710349 Review.
-
Organelle interplay in peroxisomal disorders.Trends Mol Med. 2009 Jul;15(7):293-302. doi: 10.1016/j.molmed.2009.05.002. Epub 2009 Jun 26. Trends Mol Med. 2009. PMID: 19560974 Review.
Cited by
-
OXPHOS mutations and neurodegeneration.EMBO J. 2013 Jan 9;32(1):9-29. doi: 10.1038/emboj.2012.300. Epub 2012 Nov 13. EMBO J. 2013. PMID: 23149385 Free PMC article. Review.
-
Characterization of heterogeneous redox responses in hepatocellular carcinoma patients using network analysis.EBioMedicine. 2019 Feb;40:471-487. doi: 10.1016/j.ebiom.2018.12.057. Epub 2018 Dec 31. EBioMedicine. 2019. PMID: 30606699 Free PMC article.
-
How Supraphysiological Oxygen Levels in Standard Cell Culture Affect Oxygen-Consuming Reactions.Oxid Med Cell Longev. 2018 Sep 30;2018:8238459. doi: 10.1155/2018/8238459. eCollection 2018. Oxid Med Cell Longev. 2018. PMID: 30363917 Free PMC article. Review.
-
The Key Role of Mitochondria in Somatic Stem Cell Differentiation: From Mitochondrial Asymmetric Apportioning to Cell Fate.Int J Mol Sci. 2023 Jul 29;24(15):12181. doi: 10.3390/ijms241512181. Int J Mol Sci. 2023. PMID: 37569553 Free PMC article. Review.
-
Regulation of ATP-gated P2X channels: from redox signaling to interactions with other proteins.Antioxid Redox Signal. 2014 Aug 20;21(6):953-70. doi: 10.1089/ars.2013.5549. Epub 2013 Sep 25. Antioxid Redox Signal. 2014. PMID: 23944253 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources