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- W2084634888 abstract "Ethanol toxicity is affected by both environmental and inherited features. Since oxidative stress is an important molecular mechanism for ethanol-induced cellular damage, the concomitant exposure to ethanol and pro-oxidative or antioxidant compounds can alter its toxicity. Here, we investigate the effects of exposure to ethanol and/or diphenyl diselenide, an organochalcogen with antioxidant properties, on parameters related to oxidative stress (thiobarbituric acid reactive species-TBARS-and delta-aminolevulinate dehydratase-delta-ALA-D activity) in mouse liver and brain. In addition, the in vitro effects of ethanol and acetaldehyde on the activity of delta-ALA-D from human erythrocytes were also investigated. Both ethanol and diphenyl diselenide decreased hepatic delta-ALA-D activity and DL-dithiothreitol (DTT) reactivated this enzyme only after ethanol-induced inhibition. Moreover, ethanol increased liver TBARS levels, independently of the presence of diphenyl diselenide treatment. Brain delta-ALA-D activity and TBARS levels were not changed by ethanol or diphenyl diselenide exposure. Under in vitro conditions, acetaldehyde was a more potent inhibitor of delta-ALA-D from human erythrocytes when compared to ethanol, demonstrating a dose-dependent effect. This study indicates that (1) hepatic delta-ALA-D is a molecular target for the damaging effect of ethanol under in vivo conditions; (2) diphenyl diselenide and ethanol seem to inhibit delta-ALA-D by different mechanisms; (3) acetaldehyde, a metabolite of ethanol, is probably the main molecule responsible for the inhibitory effects of the parent compound on delta-ALA-D." @default.
- W2084634888 created "2016-06-24" @default.
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- W2084634888 date "2006-04-01" @default.
- W2084634888 modified "2023-10-16" @default.
- W2084634888 title "Effects of ethanol and diphenyl diselenide exposure on the activity of δ-aminolevulinate dehydratase from mouse liver and brain" @default.
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- W2084634888 doi "https://doi.org/10.1016/j.fct.2005.10.014" @default.
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