Studies comparing the kinetics of cysteine conjugation and protein binding of acetaminophen by hepatic microsomes from male mice.

@article{Zhou1997StudiesCT,
  title={Studies comparing the kinetics of cysteine conjugation and protein binding of acetaminophen by hepatic microsomes from male mice.},
  author={L X Zhou and Richard R. Erickson and Jordan L. Holtzman},
  journal={Biochimica et biophysica acta},
  year={1997},
  volume={1335 1-2},
  pages={
          153-60
        }
}

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This study aimed to investigate the possible beneficial effect of 2‐mercaptoethane sulphonate (MESNA), an antioxidant agent, against acetaminophen toxicity in mice.

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The data might suggest that acetaminophen hepatotoxicity results from the formation of the reactive metabolite within the endoplasmic reticulum within the centre of mouse hepatic microsomes and blocks the posttranslational modification of secretory and membrane proteins.

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Results of partitioning experiments indicate that N-acetyl-p-benzoquinone imine is a major metabolite of acetaminophen, a considerable fraction of which is rapidly reduced back toacetaminophen.

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It is suggested that alcohol enhances acetaminophen hepatotoxicity in mice and provides supportive evidence that these three alcoholic patients probably had a similar pathophysiological basis for their liver disease.