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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.
K M Milam, and
J L Byard
January 1990,
Drug metabolism and disposition: the biological fate of chemicals,
K M Milam, and
J L Byard
September 2003,
Toxicology,
K M Milam, and
J L Byard
September 1981,
Toxicology and applied pharmacology,
K M Milam, and
J L Byard
April 1980,
Toxicology and applied pharmacology,
K M Milam, and
J L Byard
January 1981,
Journal of toxicology and environmental health,
K M Milam, and
J L Byard
October 1997,
Toxicology in vitro : an international journal published in association with BIBRA,
K M Milam, and
J L Byard
December 1987,
Cell biology and toxicology,
K M Milam, and
J L Byard
January 1995,
Drug and chemical toxicology,
K M Milam, and
J L Byard
March 1999,
Biological & pharmaceutical bulletin,
K M Milam, and
J L Byard
September 1985,
Toxicology and applied pharmacology,
