Abstract

Both camptothecin and neocazinostatin cause 50% inhibition of simian virus 40 DNA synthesis in BSC-1 cells at a drug concentration of 1-0.1 µM. Uniformly prelabeled Form I simian virus 40 DNA is not converted to Form II by 100 µM camptothecin or 10 µM (10 µg/ml) neocarzinostatin, despite extensive drug-induced breakage of cellular DNA at these concentrations. Kinetic experiments examined the fate of replicative intermediates at the onset of inhibition of DNA synthesis. In the presence of 100 µg/ml neocarzinostatin, label proceeds through replicative intermediate molecules and is found largely (>75%) as Form I simian virus 40 DNA. At 100 µM camptothecin, up to 50% of newly made simian virus 40 DNA is found as a Form II-like species.