DNA crosslinking, sister-chromatid exchange and specific-locus mutations

A. V. Carrano, L. H. Thompson, D. G. Stetka, J. L. Minkler, J. A. Mazrimas, S. Fong

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Abstract

Chinese hamster overy cells were treated with the DNA-crosslinking chemicals, mitomycin C (MMC) and porfiromycin (POR), and their monofunctional derivative decarbamoyl mitomycin C (DCMMC). After exposure, the cells were studied for the induction of sister-chromatid exchanges (SCEs) and mutations at the hypoxanthine phosphoribosyltransferase and adenine phosphoribosyltransferase loc. The frequency of SCEs varied significantly in successive sampling intervals, requiring the weighting of each interval by the percentage of second-divison mitosis in that interval to obtain the mean SCE frequency for each dose. All 3 compounds were potent induceers of SCEs but weakly mutagenic. All 3 chemicals by concentration were approximately equally effective in inducing SCEs or mutations. When the induced SCEs and mutations were com-compared at equal levels of survival, DCMMC was slightly more effective than MMC or POR in inducing SCEs and somewhat less mutagenic. These results indicate that the DNA interstrand crosslink is not the major lesion responsible for the induction of SCE or mutation by these compounds.

Original languageEnglish (US)
Pages (from-to)175-188
Number of pages14
JournalMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Volume63
Issue number1
DOIs
StatePublished - 1979
Externally publishedYes

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ASJC Scopus subject areas

  • Molecular Biology
  • Health, Toxicology and Mutagenesis
  • Medicine(all)

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