{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,24]],"date-time":"2025-10-24T12:57:22Z","timestamp":1761310642141},"reference-count":46,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2010,11,16]],"date-time":"2010-11-16T00:00:00Z","timestamp":1289865600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:p>Previous reports have proposed that reactive oxygen species resulting from induction of cytochrome P450 (CYP) isozymes might be involved in the modes of action of hepatocarcinogens with CYP\u2010inducible potency. In the present study, we investigated 8\u2010hydroxydeoxyguanosine (8\u2010OHdG) levels, <jats:italic>in vivo<\/jats:italic> mutagenicity and glutathione <jats:italic>S<\/jats:italic>\u2010transferase placental form (GST\u2010P)\u2010positive foci in the livers of <jats:italic>gpt<\/jats:italic> delta rats treated with piperonyl butoxide (PBO) or phenobarbital (PhB) for 4 and 13\u2003weeks. Significant elevations in <jats:italic>Cyp 1A1<\/jats:italic> and <jats:italic>Cyp 1A2<\/jats:italic> mRNA levels after PBO treatment, and in <jats:italic>Cyp 2B1<\/jats:italic> mRNA levels after PBO or PhB treatment, appeared together with remarkable hepatomegaly through the experimental period. Time\u2010dependent and statistically significant increases in 8\u2010OHdG levels were observed in the PBO treatment group along with significant increases in proliferating cell nuclear antigen (PCNA)\u2010positive hepatocytes at 4\u2003weeks, while no increase in 8\u2010OHdG levels was found in PhB\u2010treated rats. No changes in mutant frequencies of <jats:italic>gpt<\/jats:italic> and <jats:italic>red\/gam<\/jats:italic> (Spi<jats:sup>\u2010<\/jats:sup>) genes in liver DNA from PBO\u2010 or PhB\u2010treated rats were observed at 4 or 13\u2003weeks. A 13\u2010week exposure to either PBO or PhB did not affect the number and area of GST\u2010P\u2010positive hepatocytes. CYP 1A1 and 1A2 induction may be responsible for elevated levels of 8\u2010OHdG in PBO\u2010treated rats. However, neither GC:TA transversions nor deletion mutations, typically regarded as 8\u2010OHdG\u2010related mutations, were observed in any of the treated rats. We conclude that reactive oxygen species, possibly produced through CYP catalytic pathways, likely induced genomic DNA damage but did not give rise to permanent gene mutation. 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