Evidence that mAMSA induces topoisomerase action.
Evidence is presented that the topoisomerase inhibitors novobiocin and coumermycin inhibit the production of double-strand breaks in mouse mastocytoma cell nuclear DNA by the anticancer drug 4'[(9-acridinyl)amino]-methanesulphon-m-anisidide (mAMSA). Novobiocin did not inhibit resealing of DNA breaks induced by mAMSA. It is suggested that mAMSA intercalation into DNA induces the action of a type II topoisomerase. mAMSA and oAMSA were equally effective in breaking the DNA in isolated nuclei.
D000609:Aminoacridines / Q000494:pharmacology*; D049933:Aminocoumarins; D000677:Amsacrine; D000818:Animals; D002460:Cell Line; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism*; D003374:Coumarins / Q000494:pharmacology; D004264:DNA Topoisomerases, Type I / Q000378:metabolism*; D004273:DNA, Neoplasm / Q000378:metabolism; D007364:Intercalating Agents / Q000494:pharmacology*; D007700:Kinetics; D012515:Mast-Cell Sarcoma / Q000378:metabolism*; D051379:Mice; D009675:Novobiocin / Q000494:pharmacology; D012513:Sarcoma, Experimental / Q000378:metabolism
D000609:Aminoacridines; D049933:Aminocoumarins; D003374:Coumarins; D004273:DNA, Neoplasm; D007364:Intercalating Agents; D000677:Amsacrine; D009675:Novobiocin; D004264:DNA Topoisomerases, Type I; C004628:coumermycin