Differential effect of covalent protein modification and glutathione depletion on the transcriptional response of Nrf2 and NF-kappaB.

ABSTRACT: Liver injury associated with exposure to therapeutic agents that undergo hepatic metabolism can involve the formation of reactive metabolites. These may cause redox perturbation which can result in oxidative stress as well as protein modification leading to activation or inhibition of cellular transcriptional responses. Nevertheless, the effects of these challenges on more than one transcriptional pathway simultaneously remain unclear. We have investigated two transcription factors known to be sensitive to electrophilic stress and redox perturbation, Nrf2 and NF-kappaB, in mouse liver cells. Cellular stress was induced by the probes: N-acetyl-p-benzoquinineimine (NAPQI), the reactive metabolite of acetaminophen; dinitrochlorobenzene (DNCB), a model electrophile; and buthionine (S,R)-sulfox

SUBMITTER: Chia AJ 

PROVIDER: S-EPMC2884179 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature