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Titolo:
Protective effect of carvedilol on chenodeoxycholate induction of the permeability transition pore
Autore:
Rolo, AP; Oliveira, PJ; Moreno, AJM; Palmeira, CM;
Indirizzi:
Univ Coimbra, Dept Zool, Ctr Neurosci & Cell Biol, P-3001517 Coimbra, Portugal Univ Coimbra Coimbra Portugal P-3001517 iol, P-3001517 Coimbra, Portugal
Titolo Testata:
BIOCHEMICAL PHARMACOLOGY
fascicolo: 11, volume: 61, anno: 2001,
pagine: 1449 - 1454
SICI:
0006-2952(20010601)61:11<1449:PEOCOC>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
LIVER MITOCHONDRIAL BIOENERGETICS; ELECTRON-TRANSPORT CHAIN; ISOLATED RAT HEPATOCYTES; BILE-ACID TOXICITY; CYCLOSPORINE-A; HEART-MITOCHONDRIA; MECHANISM; CHOLESTASIS; MEMBRANE; MODULATION;
Keywords:
chenodeoxycholic acid; carvedilol; BM-910228; liver mitochondria; permeability transition; cardiomyopathy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Palmeira, CM Univ Coimbra, Dept Zool, Ctr Neurosci & Cell Biol, P-3001517 Coimbra, Portugal Univ Coimbra Coimbra Portugal P-3001517 7 Coimbra, Portugal
Citazione:
A.P. Rolo et al., "Protective effect of carvedilol on chenodeoxycholate induction of the permeability transition pore", BIOCH PHARM, 61(11), 2001, pp. 1449-1454

Abstract

Intracellular accumulation of toxic, hydrophobic bile acids has been proposed as one of the putative final common pathways leading to cholestatic liver injury. Furthermore, bile acids have been proposed as a causative factorfor hepatic cardiomyopathy. Hepatic tissue concentrations of chenodeoxycholic acid (CDCA) during cholestasis are greater than those of other toxic bile acids. In the presence of calcium and phosphate, CDCA induced the permeability transition pore (PTP) in freshly isolated rat liver mitochondria. Inthis study, we evaluated the effects of carvedilol, a multirole cardioprotective compound, on CDCA-induced PTP. Mitochondrial membrane potential, osmotic swelling, and calcium fluxes were monitored. CDCA-induced PTP, characterized by membrane depolarization, release of matrix calcium, and osmotic swelling, was prevented by carvedilol. Under the same conditions, its hydroxylated analog BM-910228 did not reveal any protective effect. This finding reinforces carvedilol's therapeutic interest, because it may potentially prevent mitochondrial dysfunction associated with cardiomyopathy in the pathophysiology of cholestatic liver disease. (C) 2001 Elsevier Science Inc. Allrights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 06:44:36