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Title

Differential role of ethanol and acetaldehyde in the induction of oxidative stress in Hep G2 cells: Effect on transcription factors AP-1 and NF-κB

AuthorsRomán, Juan; Colell Riera, Anna ; Blasco, Carmen; Caballería, Juan; Parés, Albert; Rodés, Joan; Fernández-Checa, José C.
Issue Date1999
PublisherJohn Wiley & Sons
CitationHepatology 30(6): 1473-1480 (1999)
AbstractThe 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-κB (NF-κB) 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 μmol/L) caused oxidative stress in HepG2 cells, an effect that was independent of blocking reduced glutathione (GSH) synthesis with buthionine-L-sulfoximine (BSO). However, BSO preincubation caused an overproduction of peroxides and activation of NF-κB and AP-1 in E47 cells even in the absence of ethanol. Furthermore, the incubation of E47 cells with ethanol (80 mmol/L for up to 5 days) depleted cellular GSH stores in both cytosol and mitochondria, reflecting the induction of oxidative stress. Ethanol activated NF-κB 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-κB and AP-1; in contrast, ethanol failed to activate these transcription factors in HepG2. Thus, our findings indicate that activation of NF-κB and AP-1 by ethanol and acetaldehyde occurs through distinct mechanisms. CYP2E 1 is indispensable in the induction of oxidative stress from ethanol, whereas the activation of NF- κB and AP-1 by acetaldehyde is independent of oxidative stress.
Publisher version (URL)http://dx.doi.org/10.1002/hep.510300623
URIhttp://hdl.handle.net/10261/111564
DOI10.1002/hep.510300623
Identifiersdoi: 10.1002/hep.510300623
issn: 0270-9139
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