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Titolo:
Acidosis promotes the permeability transition in energized mitochondria: Implications for reperfusion injury
Autore:
Kristian, T; Bernardi, P; Siesjo, BK;
Indirizzi:
Univ Maryland, Dept Anesthesiol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 Anesthesiol, Baltimore, MD 21201 USA Queens Med Ctr, Inst Neurosci, Ctr Study Neurol Dis, Honolulu, HI USA Queens Med Ctr Honolulu HI USA i, Ctr Study Neurol Dis, Honolulu, HI USA Univ Padua, CNR, Unit Study Biomembranes, I-35100 Padua, Italy Univ PaduaPadua Italy I-35100 Study Biomembranes, I-35100 Padua, Italy Univ Padua, Dept Biomed Sci, I-35100 Padua, Italy Univ Padua Padua ItalyI-35100 ua, Dept Biomed Sci, I-35100 Padua, Italy
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 10, volume: 18, anno: 2001,
pagine: 1059 - 1074
SICI:
0897-7151(200110)18:10<1059:APTPTI>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-LIVER MITOCHONDRIA; FOCAL CEREBRAL-ISCHEMIA; CYCLOSPORINE-A; BRAIN-DAMAGE; HEART-MITOCHONDRIA; FOREBRAIN ISCHEMIA; PHOSPHATE CARRIER; CYTOCHROME-C; CELL-DEATH; SHORT-TERM;
Keywords:
brain mitochondria; heart mitochondria; mitochondrial permeability transition; pH; phosphate;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Kristian, T Univ Maryland, Dept Anesthesiol, 685 W Baltimore St,MSTF 5-34,Baltimore, MD 21201 USA Univ Maryland 685 W Baltimore St,MSTF 5-34 Baltimore MD USA 21201
Citazione:
T. Kristian et al., "Acidosis promotes the permeability transition in energized mitochondria: Implications for reperfusion injury", J NEUROTRAU, 18(10), 2001, pp. 1059-1074

Abstract

We have studied the influence of pH on opening of the mitochondrial permeability transition pore (PTP) in both deenergized and energized mitochondria. in the presence of P-i. In deenergized mitochondria from rat brain and heart, we observed the expected inhibition of Ca2+-induced PTP opening at increasingly acidic pH values. Unexpectedly, mitochondria energized with either electron transport complex I or complex II substrates displayed the opposite behavior, acidic pH promoting rather than inhibiting PTP opening. We show that the potentiating effect of acidic pH is due to an increased rate ofP-i uptake. The data also revealed that brain mitochondria are more heterogeneous than heart or liver mitochondria in relation to onset of a permeability transition, and that this heterogeneity depends on their P-i transportcapacity. Taken together, these results indicate that the inhibitory effects of acidic pH on the PTP may be overcome in situ by an increased rate of Pi uptake, and that ischemic and postischemic acidosis may worsen rather than relieve PTP-dependent tissue damage.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 12:30:53