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- W76872398 abstract "It has been presumed that DNA repair proceeds efficiently to remove alkyl lesions from DNA and protect cells at low levels of environmental exposure. Thus, cells would be at major risk only as this capacity for repair is saturated. According to such a scheme, cells, particularly non-dividing cells, would not be expected to accumulate lesions at low levels of alkylation. This prediction is at odds with the natures of the risks for carcinogenesis and cellular aging. Most measurements of repair of such simple DNA lesions as methyl groups have employed higher levels of damage for convenience of detection. The authors have used the highly sensitive (/sup 32/P)-postlabeling technique of Randerath, et al. to study repair of 7 methylguanine (7MG) at two levels of damage by methylnitrosourea (MNU). Mouse fibroblasts (L929) were grown with (/sup 3/H)-thymidine to label the DNA, and, at confluency, were exposed to MNU at varying doses. At 1 mM, an average of six 7MG's were identified per 10/sup 5/ DNA bases. Less than 10% were removed by 24 hrs. In contrast, at 5 mM there were 16.2 7MG's per 10/sup 5/ nucleotides, and 53% were removed by 24 hrs. This finding, that contact inhibited cells did notmore » remove low levels of 7MG efficiently, suggests that they could accumulate such lesions from low levels of toxic exposure. Although 7MG is not considered a carcinogenic insult, this type of accumulation of DNA lesions from low levels of exposure could account for such chronic effects as cellular aging and carcinogenesis.« less" @default.
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- W76872398 date "1986-05-01" @default.
- W76872398 modified "2023-09-26" @default.
- W76872398 title "Apparent threshold for repair of 7 methylguanine in contact inhibited mouse fibroblasts" @default.
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