Hydrazine and the Methylation of DNA Guanine
Abstract
Earlier studies demonstrated that hydrazine administration to rodents results in the methylation of liver DNA guanine and that S-adenosylmethionine was the apparent methyl donor in this response. The present study characterized the hamster as an animal model in a study of the methylation response to acute and subchronic exposures to hydrozine and has examined further the possible roles S-adenosylmethionine and the 1-carbon pool may have in the methylation of liver DNA guanine in hydraine-poisoned animals. The hamster is more resistant that rate or mouse to the acute toxicity of hydrasine and can tolerate up to 120 mg hydrazine/kg body wt per os. The amounts of 7-methylguanine that formed in liver DNA changed little when the dose of hydrazine (<45 mg/kg) produced little cytotoxicity; however, at higher doses (>60 mg/kg) the formation of these aberrant basses in liver DNA increased greatly, as did the cytotoxicity in the liver. The rate of formation of these bases after administration of 90 mg hydrazine/kg body wt was rapid and 06-methylguanine persisted in hamster liver DNA longer than it did in rat liver DNA, suggesting that repeated doses of hydrazine to the hamster may force an accumulation of the promutagenic lesion in the DNA.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 1983
- Accession Number
- ADA132944
Entities
People
- Ronald C. Shank
- William S. Bosan
Organizations
- University of California, Irvine