Changes in glutathione in acute and chronic alcohol intoxication

@article{Guerri1980ChangesIG,
  title={Changes in glutathione in acute and chronic alcohol intoxication},
  author={Consuelo Guerri and Santiago Grisol{\'i}a},
  journal={Pharmacology Biochemistry and Behavior},
  year={1980},
  volume={13},
  pages={53-61},
  url={https://api.semanticscholar.org/CorpusID:28101988}
}
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FACTORS INVOLVED IN HEPATIC GLUTATHIONE DEPLETION INDUCED BY ACUTE ETHANOL ADMINISTRATION

    Dal W. Choi, Sung Y. Kim, Sang K. Kim, Young C. Ki
    Medicine, Biology
  • 2000
In the liver of rats treated acutely with ethanol, glutathione efflux plays the most important role in the reduction of this tripeptide, which would be aggravated by a transient decrease in glutathion synthesis and by increased consumption in association with its metabolism.

Factors involved in hepatic glutathione depletion induced by acute ethanol administration.

Glutathione efflux plays the most important role in the reduction of this tripeptide in the liver of rats treated acutely with ethanol, which would be aggravated by a transient decrease in glutathione synthesis and by increased consumption in association with its metabolism.

Increased plasma levels of glutathione and malondialdehyde after acute ethanol ingestion in humans.

Glutathione depletion and recovery after acute ethanol administration in the aging mouse.

Decreased hepatic glutathione in chronic alcoholic patients.

Chronic ethanol consumption affects glutathione status in rat liver.

Chronic ethanol consumption by well-nourished rats for 6 wk increased enzyme activities related to the recycling and utilization of glutathione in the liver, suggesting an enhancement in the activities of the hepatic antioxidative defense system may be one of the protective mechanisms of the body against oxidative tissue damage caused by ethanol-induced free radicals.

Increased acetaminophen-induced hepatotoxicity after chronic ethanol consumption in mice.

Increased hepatic efflux of glutathione after chronic ethanol feeding.

Effects of chronic ethanol feeding on glutathione turnover in the rat.

Alterations in hepatic metabolism of sulfur-containing amino acids induced by ethanol in rats

The results show that a single dose of ethanol induces profound changes in hepatic S-amino acid metabolism, some of which persist for several days, and Ethanol not only inhibits the cysteine synthesis but suppresses the Cysteine availability further by enhancing its irreversible catabolism to taurine, which would play a significant role in the depletion of hepatic GSH.
...

46 References

Increased biliary glutathione disulfide release in chronically ethanol‐treated rats

Effect of acute ethanol intoxication on the content of reduced glutathione of the liver in relation to its lipoperoxidative capacity in the rat

Effect of ethanol on glutathione concentration in isolated hepatocytes.

The hypothesis that acetaldehyde is responsible for the depletion of GSH induced by ethanol is supported and methionine prevents the effect of alcohol or acetaldehyde on GSH concentration in hepatocytes.

The influence of prolonged ethanol intake on the levels and turnover of alcohol and aldehyde dehydrogenases and of brain (Na + K)-ATPase of rats.

To ascertain whether synthesis or degradation of these enzymes were responsible for the marked increase in activity the turnover of several liver fractions and of the indicated enzymes were measured by the dual-labelled isotope technique.

Animal models of ethanol dependence and liver injury in rats and baboons.

In showing that all aspects of liver injury observed in alcoholics can be reproduced in animals by the feeding of pure ethanol with an adequate diet, this study incriminates ethanol itself as a cause for the hepatic complications.

Influence of prolonged ethanol intake on the levels and turnover of alcohol and aldehyde dehydrogenases and glutathione.

It is believed that acute toxicity results from acidotic effects arising from aldehyde fromation and its oxidation to formic acid and that formaldehyde interfers with the generation of ATP during oxidative phosphorylation, which results in loss of vision.

High blood acetaldehyde levels after ethanol administration. Difference between alcoholic and nonalcoholic subjects.

The ethanol concentration at which this fall of blood acetaldehyde occurred suggests desaturation of an ethanol oxidizing system other than alcohol dehydrogenase and indicates that at high ethanol blood levels, such a system contributes to ethanol oxidation.

A possible mechanism for the peroxidation of lipids due to chronic ethanol ingestion.

A possible protective role for sulphydryl compounds in acute alcoholic liver injury.

Species differences in hepatic glutathione depletion, covalent binding and hepatic necrosis after acetaminophen.