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.