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• W2111401978 abstract "Background Chronic ethanol ( E t OH ) administration to experimental animals induces hepatic oxidative stress and up‐regulates mitochondrial biogenesis. The mechanisms by which chronic E t OH up‐regulates mitochondrial biogenesis have not been fully explored. In this work, we hypothesized that oxidative stress is a factor that triggers mitochondrial biogenesis after chronic E t OH feeding. If our hypothesis is correct, co‐administration of antioxidants should prevent up‐regulation of mitochondrial biogenesis genes. Methods Rats were fed an E t OH ‐containing diet intragastrically by total enteral nutrition for 150 days, in the absence or presence of the antioxidant N ‐acetylcysteine ( NAC ) at 1.7 g/kg/d; control rats were administered isocaloric diets where carbohydrates substituted for E t OH calories. Results E t OH administration significantly increased hepatic oxidative stress, evidenced as decreased liver total glutathione and reduced glutathione/glutathione disulfide ratio. These effects were inhibited by co‐administration of E t OH and NAC . Chronic E t OH increased the expression of mitochondrial biogenesis genes including peroxisome proliferator‐activated receptor gamma‐coactivator‐1 alpha and mitochondrial transcription factor A , and mitochondrial DNA ; co‐administration of E t OH and NAC prevented these effects. Chronic E t OH administration was associated with decreased mitochondrial mass, inactivation and depletion of mitochondrial complex I and complex IV , and increased hepatic mitochondrial oxidative damage, effects that were not prevented by NAC . Conclusions These results suggest that oxidative stress caused by chronic E t OH triggered the up‐regulation of mitochondrial biogenesis genes in rat liver, because an antioxidant such as NAC prevented both effects. Because NAC did not prevent liver mitochondrial oxidative damage, extra‐mitochondrial effects of reactive oxygen species may regulate mitochondrial biogenesis. In spite of the induction of hepatic mitochondrial biogenesis genes by chronic E t OH , mitochondrial mass and function decreased probably in association with mitochondrial oxidative damage. These results also predict that the effectiveness of NAC as an antioxidant therapy for chronic alcoholism will be limited by its limited antioxidant effects in mitochondria, and its inhibitory effect on mitochondrial biogenesis." @default.
• W2111401978 created "2016-06-24" @default.
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• W2111401978 date "2014-12-01" @default.
• W2111401978 modified "2023-10-12" @default.
• W2111401978 title "<i>N</i>-Acetylcysteine Inhibits the Up-Regulation of Mitochondrial Biogenesis Genes in Livers From Rats Fed Ethanol Chronically" @default.
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• W2111401978 doi "https://doi.org/10.1111/acer.12576" @default.
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