Response of V79 cells to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) treatment: inhibition of poly(ADP-ribose) and topoisomerase activity.
MNNG-induced killing of V79 cells has been found to be enhanced on inhibition of topoisomerase II activity by nalidixic acid and poly(ADP-ribose) polymerase synthesis by benzamide. Using these 2 inhibitors in conjunction after MNNG treatment, some overlap in the functions of these 2 enzymes was observed. Nalidixic acid and benzamide were found to suppress the yields of mutations and SCEs induced by MNNG. Benzamide was more effective in suppressing the mutation yield whereas nalidixic acid was more effective in suppressing SCEs. A model based on the relative requirement of topoisomerase and poly(ADP-ribose) for the repair of different types of damage has been proposed to explain the results.
Roy
M
M
Crystallography and Molecular Biology Division, Saha Institute of Nuclear Physics, Calcutta, India.
Ghosh
R
R
Dey
S K
SK
Bhattacharjee
S B
SB
D000246:Adenosine Diphosphate Ribose / Q000037:antagonists & inhibitors*; D000818:Animals; D001549:Benzamides / Q000494:pharmacology; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D006224:Cricetinae; D003412:Cricetulus; D008769:Methylnitronitrosoguanidine / Q000633:toxicity*; D009153:Mutagens; D009154:Mutation; D009268:Nalidixic Acid / Q000494:pharmacology; D012854:Sister Chromatid Exchange / Q000187:drug effects; D059005:Topoisomerase II Inhibitors
D001549:Benzamides; D009153:Mutagens; D059005:Topoisomerase II Inhibitors; D008769:Methylnitronitrosoguanidine; D000246:Adenosine Diphosphate Ribose; D009268:Nalidixic Acid; C037689:benzamide