Abstract
The effects of N-acetylcysteine (NAC) on the toxicity, conjugate formation, and covalent binding of acetaminophen (pHAA) and its presumed toxic metabolite were studied in suspensions of isolated mouse hepatocytes. Preincubation of liver cells with NAC prior to the addition of pHAA resulted in enhanced protection compared to the concurrent addition of pHAA and NAC, thus indicating a time lag between availability of NAC and exertion of a protective effect. Furthermore, a protective concentration of NAC caused a large increase in the proportion of pHAA plus metabolites found as the glutathione (GSH) conjugate and a decrease in covalent binding of radiolabeled pHAA metabolite to proteins. Thus, it appears that NAC protects against pHAA toxicity by increasing the availability of intracellular GSH.
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