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Titolo:
Differential role of ethanol and acetaldehyde in the induction of oxidative stress in HEP G2 cells: Effect on transcription factors AP-1 and NF-kappaB
Autore:
Roman, J; Colell, A; Blasco, C; Caballeria, J; Pares, A; Rodes, J; Fernandez-Checa, C;
Indirizzi:
CSIC, Dept Med, Liver Unit, Barcelona, Spain CSIC Barcelona SpainCSIC, Dept Med, Liver Unit, Barcelona, Spain CSIC, Dept Med, Liver Unit, Barcelona 08036, Spain CSIC Barcelona Spain 08036 Dept Med, Liver Unit, Barcelona 08036, Spain CSIC, Inst Invest Biomed August Pi Suner, Barcelona 08036, Spain CSIC Barcelona Spain 08036 iomed August Pi Suner, Barcelona 08036, Spain
Titolo Testata:
HEPATOLOGY
fascicolo: 6, volume: 30, anno: 1999,
pagine: 1473 - 1480
SICI:
0270-9139(199912)30:6<1473:DROEAA>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; GAMMA-GLUTAMYLCYSTEINE SYNTHETASE; INDUCED LIPID-PEROXIDATION; ELECTRON-TRANSPORT CHAIN; HEAVY SUBUNIT CHAIN; MITOCHONDRIAL GLUTATHIONE; ALCOHOL-DEHYDROGENASE; CYTOCHROME-P450 2E1; REDUCED GLUTATHIONE; GENE-TRANSCRIPTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Fernandez-Checa, C Hosp Clin & Prov Villarroel, CSIC, Liver Unit, Inst Invest Biomed, 170, Barcelona 08036, Spain Hosp Clin & Prov Villarroel 170 Barcelona Spain 08036
Citazione:
J. Roman et al., "Differential role of ethanol and acetaldehyde in the induction of oxidative stress in HEP G2 cells: Effect on transcription factors AP-1 and NF-kappaB", HEPATOLOGY, 30(6), 1999, pp. 1473-1480

Abstract

The oxidative metabolism of ethanol by the cytochrome P450 2E1 (CYP2E1) has been recognized to contribute to the ethanol-induced deleterious effects through the induction of oxidative stress. This study compared the effect of ethanol and acetaldehyde in the induction of oxidative stress and activation of transcription factors nuclear factor-kappa B (NF-kappa B) and activating protein 1 (AP-1) in HepG2 cells, which do not express CYP2E1, and HepG2 cells transfected with CYP2E1 (E47 cells), Neither ethanol (80 mmol/L) nor acetaldehyde (25-200 mu mol/L) caused oxidative stress in HepG2 cells, aneffect that was independent of blocking reduced glutathione (GSH) synthesis with buthionine-L-sulfoximine (BSO), However, BSO preincubation caused anoverproduction of peroxides and activation of NF-kappa B and AP-1 in E47 cells even in the absence of ethanol, Furthermore, the incubation of E47 cells with ethanol (80 mmoI/L for up to 4 days) depleted cellular GSH stores in both cytosol and mitochondria, reflecting the induction of oxidative stress, Ethanol activated NF-kappa B and AP-1 in E47 cells, an effect that was prevented by 4-methylpyrazole, potentiated by cyanamide, and attenuated by trolox C, Interestingly, however, despite the inability of acetaldehyde to induce oxidative stress in HepG2, acetaldehyde activated NF-kappa B and AP-1; in contrast, ethanol failed to activate these transcription factors in HepG2. Thus, our findings indicate that activation of NF-kappa B and AP-1 byethanol and acetaldehyde occurs through distinct mechanisms. CYP2E1 is indispensable in the induction of oxidative stress from ethanol, whereas the activation of NF-kappa B and AP-1 by acetaldehyde is independent of oxidative stress.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 16:02:11