Chronic ethanol consumption affects glutathione status in rat liver.

@article{Oh1998ChronicEC,
  title={Chronic ethanol consumption affects glutathione status in rat liver.},
  author={Supa Oh and C. I. Kim and H. J. Chun and S C Park},
  journal={The Journal of nutrition},
  year={1998},
  volume={128 4},
  pages={
          758-63
        }
}
There is no consensus yet on the role of oxidative stress in the nutritional outcome of chronic ethanol feeding and the status of cellular antioxidative defense systems against ethanol toxicity. In this study, chronic alcohol consumption in humans was reproduced in Sprague-Dawley rats to investigate the effect of ethanol ingestion on the regulation of oxidative stress in liver with a special focus on glutathione. Adult male rats were given 36% of total energy as alcohol in the Lieber-DeCarli… 
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TLDR
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TLDR
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Effect of Zinc on Hepatic Drug Metabolism under Ethanol Toxicity
TLDR
Zinc was able to normalize the effects of ethanol in the liver, which was accredited to the antioxidant potential of zinc, as well as its ability to induce metallothionein content, which provide protection against the toxic effects of alcohol.
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TLDR
Taurine has a restorative effect on ethanol-induced hepatic damage by decreasing oxidative stress, and is proposed to have a protective effect on the prooxidant-antioxidant state following chronic ethanol treatment.
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TLDR
It is demonstrated that β-carotene improved the cell viability of hepatocytes, and increased catalase activities and glutathione levels in hepatocytes from chronically ethanol-fed rats.
Effects of b-carotene on cell viability and antioxidant status of hepatocytes from chronically ethanol-fed rats
TLDR
It is demonstrated that b-carotene improved the cell viability of hepatocytes, and increased catalase activities and glutathione levels in hepatocytes from chronically ethanol-fed rats.
Effect of zinc on hepatic lipid peroxidation and antioxidative enzymes in ethanol‐fed rats
TLDR
Interestingly, zinc treatment to rats given ethanol was able to bring down the elevated levels of SOD, catalase and GPx to within normal limits, However, zinc administration alone did not cause any significant alteration in the activities of these antioxidative enzymes.
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