Acetaminophen metabolism, cytotoxicity, and genotoxicity in rat primary hepatocyte cultures

Toxicol Appl Pharmacol. 1985 Jun 30;79(2):342-7. doi: 10.1016/0041-008x(85)90356-4.

Abstract

Acetaminophen (APAP) metabolism, cytotoxicity, and genotoxicity were measured in primary cultures of rat hepatocytes. Although 3 mM APAP caused a slight increase in cellular release of lactate dehydrogenase into the culture medium, cellular glutathione concentration (an index of APAP metabolism) was reduced by 50%. APAP at 7 mM was significantly more toxic to these hepatocytes and had a similar but more marked effect on glutathione concentrations. In spite of its cytotoxicity, neither dose of APAP stimulated DNA repair synthesis when monitored by the rate of incorporation of [3H]thymidine into DNA following exposure to APAP. Thus, although APAP has been shown to be both hepato- and nephrotoxic in several in vivo and in vitro systems, the reactive toxic metabolite of APAP is not genotoxic in rat primary hepatocyte cultures.

MeSH terms

  • Acetaminophen / metabolism*
  • Acetaminophen / toxicity
  • Aflatoxin B1
  • Aflatoxins / toxicity
  • Analysis of Variance
  • Animals
  • Colorimetry
  • Cytotoxins / metabolism*
  • Cytotoxins / toxicity
  • DNA / analysis
  • DNA Repair / drug effects
  • Glutathione / analysis
  • In Vitro Techniques
  • L-Lactate Dehydrogenase / biosynthesis
  • Liver / drug effects
  • Liver / metabolism*
  • Male
  • Rats
  • Rats, Inbred Strains
  • Thymidine / metabolism
  • Tritium

Substances

  • Aflatoxins
  • Cytotoxins
  • Tritium
  • Acetaminophen
  • DNA
  • Aflatoxin B1
  • L-Lactate Dehydrogenase
  • Glutathione
  • Thymidine