title: Mitochondrial oxidative stress after global brain ischemia in rats.
abstract: Vulnerable neurons in the hippocampus die 2-3 days after transient global brain ischemia. In the present study, rat brain mitochondria were isolated at different time points (4 h, 24 h and 48 h) after transient global ischemia. Detection of mitochondrially-generated reactive oxygen species, measured through dichlorodihydrofluorescein oxidation, was increased up to 40% relative to control in hippocampal mitochondria at 4 h and 48 h of reperfusion. Ischemia-stimulated oxidative stress was observed with mitochondria oxidizing substrates linked to nicotinamide adenine dinucleotide or flavin adenine dinucleotide, but not in the presence of the respiratory chain inhibitor antimycin A. A slightly decreased Ca(2+) uptake capacity was observed in hippocampal mitochondria during reperfusion. We conclude that transient brain ischemia induces oxidative stress in hippocampal mitochondria.
authors.affiliation: Laboratory for Experimental Brain Research, Wallenberg Neuroscience Center, Lund University, Sölvegatan 17, S-223 62, Lund, Sweden. hans.friberg@helsingborgslasarett.se
authors.forename: Hans
authors.initials: H
authors.lastname: Friberg
authors.forename: Tadeusz
authors.initials: T
authors.lastname: Wieloch
authors.forename: Roger F
authors.initials: RF
authors.lastname: Castilho
mesh_terms: D000818:Animals; D000968:Antimycin A / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006624:Hippocampus / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000032:analysis*; D013997:Time Factors
chemical_list: D004791:Enzyme Inhibitors; D017382:Reactive Oxygen Species; D000968:Antimycin A; D002118:Calcium