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It has been known that the damage of DNA caused by the effect of alkylating agents is restored by its own repairing mechanisms. Consequently it is probable that sensitivity of the tumor cells to alkylating agents should depend at least partially on the potency of DNA repairing activity of the cells. We reported earlier1) that the acquired resistance of Yoshida sarcoma to nitrogen mustard (HN2) is due to decreased transport of the agents through the cell membrane, but there is no difference in the transport between two lines of rat ascites hepatomas, AH-13 and AH-44, which are naturally sensitive and resistnt to nitrogen mustard, respectively. Recently, Kann et al.2) reported that 2-chloroethyl isocyanate, a metabolic product, of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), inhibits repair of DNA damage of L-1210 cells produced by X-irradiation. This communication deals with the effect of nitrogen mustard with concomitant use of 2chloroethyl isocyanate on a HN2-resistant line of hepatoma, AH-44. The enhancement of cytotoxic effect of HN2 by this DNA-repair inhibitor was proved by the following experiment. Intraperitoneal injection of either 0.05mg/kg of HN2 or 5mg/kg of BCNU to Donryu rats bearing AH-44 does not produce life prolongation but, as shown in Fig. 1, the combined use of both agents in the same doses showed a remarkable effect. By the combined treatment of the same tumor with, 0.05mg/kg of HN2 and 50mg/kg of 2-chloroethyl isocyanate, the tumor-bearing rats survived nearly twice longer than the control, as shown in Fig. 2. The treatment by the same dose of 2-chloroethyl isocyanate alone was almost ineffective. The smear preparation of the tumor cells treated by 0.05mg/kg of HN2 alone showed

Combined effect of nitrogen mustard and DNA repair inhibitor on the resistant tumor.