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Titolo:
MITOCHONDRIAL GENERATION OF REACTIVE OXYGEN SPECIES AFTER BRAIN ISCHEMIA IN THE RAT
Autore:
PIANTADOSI CA; ZHANG J;
Indirizzi:
DUKE UNIV,MED CTR,DEPT MED,BOX 3315 DURHAM NC 27710
Titolo Testata:
Stroke
fascicolo: 2, volume: 27, anno: 1996,
pagine: 327 - 331
SICI:
0039-2499(1996)27:2<327:MGOROS>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYDROXYL RADICAL GENERATION; HEART-MITOCHONDRIA; MICRODIALYSIS; REPERFUSION; INJURY; CHAIN; ASSAY; ACID;
Keywords:
CEREBRAL ISCHEMIA, TRANSIENT; OXYGEN RADICAL; REPERFUSION; RATS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
27
Recensione:
Indirizzi per estratti:
Citazione:
C.A. Piantadosi e J. Zhang, "MITOCHONDRIAL GENERATION OF REACTIVE OXYGEN SPECIES AFTER BRAIN ISCHEMIA IN THE RAT", Stroke, 27(2), 1996, pp. 327-331

Abstract

Background and Purpose Brain mitochondria have a substantial capacityto generate reactive oxygen species after ischemia when the components of the respiratory chain are reduced and molecular oxygen is present. We tested the hypothesis that brain mitochondria in vivo produce reactive oxygen species after ischemia/reperfusion (IR) in rats at a ratesufficient to escape endogenous antioxidant defenses. Methods Ischemia-dependent production of hydroxyl radical in the hippocampus of the anesthetized rat was monitored with the use of intracerebral microdialysis. Transient global ischemia was produced by bilateral carotid artery occlusion and hemorrhagic hypotension to a mean arterial pressure of35 mm Hg for 15 minutes followed by reperfusion for 60 minutes: Salicylic acid was infused into the hippocampus during the experiments, andchanges in the recovery of its hydroxylated product, 2,3-dihydroxybenzoic acid (2,3-DHBA), were used to assess the effects of inhibitors ofmitochondrial complex I on formation of hydroxyl radical during IR. Hydroxylation data from control groups of animals were compared with data from animals undergoing IR during treatment with either a mitochondrial complex I inhibitor alone or the inhibitor plus succinic acid. Results Transient ischemia led to a fivefold increase in the recovery of2,3-DHBA by microdialysis after 1 hour relative to control animals (P<.05). Inhibition of mitochondrial complex I prevented 2,3-DHBA formation after IR; this effect could be reversed by infusion of succinic acid by microdialysis during IR.Conclusions The data indicate that reactive oxygen species generated by mitochondrial electron transport escape cellular antioxidant defenses and promote highly damaging hydroxyl radical activity after transient brain ischemia in the rat.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 13:58:58