Inhibition of post-replication repair by isonicotinic acid hydrazide.
In the presence of the alkylating mutagen N-methyl-N-nitrosourea (MNU), the well-known tuberculostatic ionicotinic acid hydrazide (INH), even in otherwise ineffective doses, depressed cell number and mitotic index in peripheral human lymphocytes and inhibited the post-replication repair process in Chinese hamster cells (CHO). INH had no influence on unscheduled DNA synthesis (cut-and-patch repair), which was negligible in CHO cells under our conditions.
D002452:Cell Count; D002460:Cell Line; D002499:Centrifugation, Density Gradient; D004247:DNA / Q000032:analysis; D004260:DNA Repair / Q000187:drug effects*; D003864:Depression, Chemical; D006801:Humans; D007538:Isoniazid / Q000494:pharmacology*; D008214:Lymphocytes / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D008938:Mitosis
D004247:DNA; D007538:Isoniazid