Abstract
This study was designed to assess, qualitatively and quantitatively, the methylation of hepatic DNA isolated from specific chromatin fractions following exposure to carcinogenic alkylating agents, methylnitrosourea (MNU), or dimethylnitrosamine (DMN). Male Sprague-Dawley rats were exposed to 0.15 mmol:kg [ methyl- 3H]MNU (10 mCi/mmol) or to 0.08 mmol/kg [ methyl- 14C]DMN (1.0 mCi/mmol) via gastric intubation. Alkylation of hepatic DNA was assessed at 3, 24, 72, and 168 hr postintubation. Hepatic chromatin was fractionated into portions having characteristics of template-active euchromatin (S2) and template-repressed heterochromatin (P2) by digestion with DNase II followed by MgCl 2 precipitation. At times of peak alkylation following the administration of either carcinogen, the S2/P2 DNA alkylation ratio was greater than 1.0 indicating that alkylation was nonrandom. In addition, the S2/P2 DNA alkylation ratio at peak alkylation following MNU treatment was 1.6 times the DMN ratio, suggesting qualitative differences between DMN- versus MNU-induced alkylation.
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