alpha-Tocopherol, MDA-HNE and 8-OHdG levels in liver and heart mitochondria of adriamycin-treated rats fed with alcohol-free beer.

Different studies indicate that oxidative stress and mitochondrial damage are key factors in different pathogenic process. The aim of this study was to investigate the possible protective role of alcohol-free beer on adriamycin-induced (ADR) heart and liver toxicity using biomarkers of oxidative stress. This effect was compared with the effect of alcohol beer intake and with a control group. Rats were randomly divided into six groups. The first group received no adriamycin, was fed with water and was regarded as the control group; the second group was injected with a ADR (two cycles of 5mg/kg); the third and fourth groups were fed with alcohol-free and beer for 21 days, respectively and the fifth and sixth groups were fed with alcohol-free and beer beginning 7 days before the administration of a first dose of ADR. Beer was administrated intragastrically and ADR (two cycles of 5mg/kg) was intraperitoneally. The levels of MDA+4HNE (malondialdehyde and 4-hydroxynonenal) in heart mitochondria was higher in the group treated with ADR alone than in the control groups, and it was lower in the groups treated with ADR that drank beer than in the ADR group alone. However, no difference was observed in liver mitochondria between the group treated with ADR and the group treated with ADR that drank beer. Significant decrease in the levels of heart and liver alpha-tocopherol was observed in the ADR group when compared to the control groups, and this decrease was normalized by beer treatment. Interestingly, the levels of antioxidant alpha-tocopherol in liver were significantly higher in rats that consumed alcohol-free beer than in those that consumed alcohol beer. Intake of alcohol-free beer showed a DNA protective effect to decreases significantly the levels of 8-OHdG levels in heart and liver increased by the ADR-treatment. In conclusion, this study clearly indicated that alcohol-free beer consumption significantly reduces the adriamycin-induced oxidative stress.