Methyl methanesulfonate adduct formation and repair in the DHFR gene and in mitochondrial DNA in hamster cells.
Chinese hamster ovary CHO-B11 cells were exposed to methyl methanesulfonate (MMS) and the formation and repair of N-methylpurines were measured in the endogenous dihydrofolate reductase (DHFR) gene domain and in mitochondrial DNA by alkaline hydrolysis which generates strand breaks at apurinic (AP) sites formed after neutral depurination. The initial levels of damage in the transcriptionally active DHFR gene, 3'-flanking non-transcribed region and in mitochondrial DNA were slightly different; the highest level of damage was in mitochondrial DNA, the lowest in the DHFR gene. The rate of adduct removal was similar in all three DNA regions examined. We conclude that there is no preferential repair of MMS induced N-methylpurines under these conditions, and that these lesions are efficiently removed from mitochondrial DNA.
Pirsel
M
M
Cancer Research Institute, Slovak Academy of Sciences, Department of Molecular Genetics, Bratislava.
Bohr
V A
VA
D000818:Animals; D016466:CHO Cells; D006224:Cricetinae; D004260:DNA Repair; D004272:DNA, Mitochondrial / Q000378:metabolism*; D008741:Methyl Methanesulfonate / Q000378:metabolism*; D013762:Tetrahydrofolate Dehydrogenase / Q000235:genetics* / Q000378:metabolism
D004272:DNA, Mitochondrial; D008741:Methyl Methanesulfonate; D013762:Tetrahydrofolate Dehydrogenase