Inhibition of poly(ADP-ribose) synthetase potentiates cell dacarbazine cytotoxicity.
Dacarbazine induces DNA lesions in cells synthesizing new DNA. When poly(ADP-ribosylation) is inhibited with 3-aminobenzamide, repair of the dacarbazine-induced DNA lesions is reduced. This is parallelled by increased cytotoxicity. Cells pre-treated with aphidicolin (to stop DNA synthesis) are resistant to dacarbazine.
D000970:Antineoplastic Agents / Q000494:pharmacology; D016590:Aphidicolin; D001549:Benzamides / Q000494:pharmacology; D002460:Cell Line; D004247:DNA / Q000187:drug effects*; D004260:DNA Repair / Q000187:drug effects*; D003606:Dacarbazine / Q000494:pharmacology*; D004224:Diterpenes / Q000494:pharmacology; D004357:Drug Synergism; D006801:Humans; D008545:Melanoma / Q000378:metabolism*; D000067856:Poly(ADP-ribose) Polymerase Inhibitors
D000970:Antineoplastic Agents; D001549:Benzamides; D004224:Diterpenes; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D016590:Aphidicolin; D003606:Dacarbazine; C025160:3-aminobenzamide; D004247:DNA