Mitochondrial respiratory chain and free radical generation in stroke
- PMID: 16257638
- DOI: 10.1016/j.freeradbiomed.2005.07.010
Mitochondrial respiratory chain and free radical generation in stroke
Abstract
Being the second most common cause of death in the industrial countries and one of the major causes of death and disability, stroke has a great effect on public health and is the neurological disease which accounts for the largest number of hospitalizations. In order to develop new treatments, biochemical mechanisms involved in brain damage have been investigated. Among them, oxidant species generated during stroke have been implicated as critical mediators of neuronal injury in this condition, although neuroprotective roles have also been demonstrated. This review is focused on the role of the mitochondrial respiratory chain as both source and target of reactive oxygen and nitrogen species such as nitric oxide, superoxide and peroxynitrite produced in cerebral ischemia. The neuroprotective role of antioxidants or other molecules acting on the mitochondrial respiratory chain and ATP synthesis in the setting of cerebral ischemia is discussed.
Similar articles
-
Oxidative stress and its role in the pathogenesis of ischaemic stroke.Int J Stroke. 2009 Dec;4(6):461-70. doi: 10.1111/j.1747-4949.2009.00387.x. Int J Stroke. 2009. PMID: 19930058 Review.
-
Nitric oxide and peroxynitrite interactions with mitochondria.Biol Chem. 2002 Mar-Apr;383(3-4):401-9. doi: 10.1515/BC.2002.044. Biol Chem. 2002. PMID: 12033431 Review.
-
Inhibition of glutamate release by delaying ATP fall accounts for neuroprotective effects of antioxidants in experimental stroke.FASEB J. 2003 Nov;17(14):2082-4. doi: 10.1096/fj.02-1086fje. Epub 2003 Sep 18. FASEB J. 2003. PMID: 14500556
-
Neuroprotective mechanisms of cerium oxide nanoparticles in a mouse hippocampal brain slice model of ischemia.Free Radic Biol Med. 2011 Sep 15;51(6):1155-63. doi: 10.1016/j.freeradbiomed.2011.06.006. Epub 2011 Jun 12. Free Radic Biol Med. 2011. PMID: 21704154
-
Time course of post-traumatic mitochondrial oxidative damage and dysfunction in a mouse model of focal traumatic brain injury: implications for neuroprotective therapy.J Cereb Blood Flow Metab. 2006 Nov;26(11):1407-18. doi: 10.1038/sj.jcbfm.9600297. Epub 2006 Mar 15. J Cereb Blood Flow Metab. 2006. PMID: 16538231
Cited by
-
Therapeutic potential of berries in age-related neurological disorders.Front Pharmacol. 2024 May 9;15:1348127. doi: 10.3389/fphar.2024.1348127. eCollection 2024. Front Pharmacol. 2024. PMID: 38783949 Free PMC article. Review.
-
The action mechanism by which C1q/tumor necrosis factor-related protein-6 alleviates cerebral ischemia/reperfusion injury in diabetic mice.Neural Regen Res. 2024 Sep 1;19(9):2019-2026. doi: 10.4103/1673-5374.390951. Epub 2023 Dec 15. Neural Regen Res. 2024. PMID: 38227531 Free PMC article.
-
Gastrodin Regulates PI3K/AKT-Sirt3 Signaling Pathway and Proinflammatory Mediators in Activated Microglia.Mol Neurobiol. 2024 May;61(5):2728-2744. doi: 10.1007/s12035-023-03743-8. Epub 2023 Nov 6. Mol Neurobiol. 2024. PMID: 37930585
-
Candidate neuroinflammatory markers of cerebral autoregulation dysfunction in human acute brain injury.J Cereb Blood Flow Metab. 2023 Aug;43(8):1237-1253. doi: 10.1177/0271678X231171991. Epub 2023 May 3. J Cereb Blood Flow Metab. 2023. PMID: 37132274 Free PMC article. Review.
-
Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases.Antioxidants (Basel). 2023 Apr 6;12(4):895. doi: 10.3390/antiox12040895. Antioxidants (Basel). 2023. PMID: 37107270 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical