Chinese hamster cells harbouring the Escherichia coli O6-alkylguanine alkyltransferase gene are less susceptible to sister chromatid exchange induction and chromosome damage by methylating agents

Clones of Chinese hamster V79 cells harbouring the Escherichia coli O6-alkylguanine (O6-AG) alkylphosphotriester (AP) alkyltransferase (ATase) gene (clone 8) or a subclone of it that codes only for O6-AG ATase activity (clone SB) have been exposed to increasing doses of N-methyl-N-nitrosourea (MNU)...

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Bibliographic Details
Published in:Carcinogenesis (New York) 1986-12, Vol.7 (12), p.2077-2080
Main Authors: White, G.R.M., Ockey, C.H., Brennand, J., Margison, G.P.
Format: Article
Language:English
Subjects:
Alkylating Agents - toxicity
Animals
Applied sciences
Biological and medical sciences
Cell Line
Chromosome Aberrations
Cricetinae
Cricetulus
Escherichia coli - genetics
Exact sciences and technology
Fundamental and applied biological sciences. Psychology
Guanine - analogs & derivatives
Guanine - toxicity
Methyl Methanesulfonate - toxicity
Methylnitrosourea - toxicity
Methyltransferases - genetics
Molecular and cellular biology
Molecular genetics
Mutagenesis. Repair
O-Methylguanine-DNA Methyltransferase
Other techniques and industries
Sister Chromatid Exchange
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Summary:Clones of Chinese hamster V79 cells harbouring the Escherichia coli O6-alkylguanine (O6-AG) alkylphosphotriester (AP) alkyltransferase (ATase) gene (clone 8) or a subclone of it that codes only for O6-AG ATase activity (clone SB) have been exposed to increasing doses of N-methyl-N-nitrosourea (MNU) or methybnethanesulphonate (MMS) and the frequencies of induced sister chromatid exchanges (SCEs) measured. In control (clone 2) cells, SCE induction was almost linearly proportional to dose of MNU or MMS and at the highest doses used (15 or 80 μg/ml) SCE frequencies were 6 or 8 times background levels, respectively. Slightly lower levels of MMS-induced SCEs were seen in clone 8 and clone SB cells whilst, in contrast, MNU-induced SCE levels in these two clones were drastically reduced being less than twice background levels at 15 μg/ml. After treatment with N-butyl-N-nitrosourea, SCE frequency was similar in all three clones. At higher doses, MNU treatment produced less chromatid aberrations and micronuclei in clone SB than in clone 2 cells. These results suggest that ATase-repairable damage is involved in the induction of SCE, chromosome aberrations and micronuclei in V79 cells.
ISSN:0143-3334
1460-2180
DOI:10.1093/carcin/7.12.2077