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Effects of Acivicin and Dipyridamole on Hepatoma 3924A Cells¹

Laboratory for Experimental Oncology, Indiana University School of Medicine, Indianapolis, Indiana 46223

Dipyridamole inhibited the incorporation of cytidine, thymidine, uridine, and guanosine in rat hepatoma 3924A cells with 50% inhibitory concentrations of 0.2 to 0.5 µM. For deoxycytidine, the 50% inhibitory concentration was about 100 times higher (23.8 µM). Addition of a combination of cytidine, deoxycytidine, and guanosine, at an optimal concentration of 80 µM each, protected the hepatoma cells from the growth-inhibitory action of the antiglutamine drug, acivicin. The protection provided by the nucleosides was blocked by dipyridamole (6 µM), but not by nitrobenzylthioinosine (30 µM). The effect on cell survival of graded concentrations of 0.25 to 1.75 µM acivicin plus dipyridamole (5 µM) and 80 µM concentrations each of cytidine, deoxycytidine, and guanosine was investigated. At an acivicin concentration of 1.75 µM, survivals in the different groups were: (a) acivicin alone, 1%; (b) acivicin plus dipyridamole, 1%; (c) acivicin plus nucleosides, 78%; and (d) acivicin plus nucleosides plus dipyridamole, 3%. Acivicin and dipyridamole were cytotoxic for hepatoma 3924A cells with 50% inhibitory concentrations of 0.5 and 20.3 µM, respectively, as measured by clonogenic assay.

¹ This investigation was supported by USPH Grants CA-13526 and CA-05034.

² Permanent address: Institute of Antibiotics, Chinese Academy of Medical Sciences, Peking, People's Republic of China.

³ To whom requests for reprints should be addressed, at the Laboratory for Experimental Oncology, Indiana University School of Medicine, Indianapolis, Ind. 46223.

Received 7/28/82. Accepted 1/11/83.