DNA-repair deficiencies do not affect intercalator-induced cytotoxicity or DNA scission in human cells.

The ability of the DNA intercalator m-AMSA to produce protein-associated DNA-strand breaks in normal, xeroderma pigmentosum and ataxia-telangiectasia fibroblasts was compared with m-AMSA uptake and cytotoxicity. No differences were detected between the cytotoxicity and DNA breakage produced by this antineoplastic acridine derivative among these three human cell lines. Uptake studies confirmed that no actual increased sensitivity was being masked by decreased intracellular drug. m-AMSA appears to be unique in its ability to produce breaks in cellular DNA that are not associated with an enhanced sensitivity in repair-deficient cells. Intercalator-induced, protein-associated DNA breaks are probably the result of a novel cellular response which differs from that which is abnormal in xeroderma pigmentosum or ataxia-telangiectasia cells.