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The anti-tumor drugcis -platinum(II)diamminodichloride (PDD) induced extensive filamentation in wild-typeEscherichia coli and in mutants lacking certain deoxyribonucleic acid (DNA) repair functions (uvrA, recB, recC , andpolA ); viability of repair-deficient mutants treated with PDD was significantly less than that of wild-type cells. PDD was highly toxic tolex1, lex1 uvrA6 (where its effect was cummulative), andrecA13 mutants, all of which were killed without formation of filaments.3 H-thymine incorporated into DNA of cells subsequently treated with PDD became trichloroacetic acid-soluble at rates similar to those observed after exposure to comparable doses of ultraviolet light (UV) or mitomycin C. PDD, like UV, induced extensive degradation of DNA inrecA organisms. After a 30-min lag, PDD inhibited significantly the synthesis of DNA but not of ribonucleic acid or protein inE. coli . However, the relative differences between rates of DNA synthesis observed in PDD-treated and control cells decreased substantially when the duration of pulses (3 H-thymine) was prolonged from 2 to 5 min. These observations suggest that PDD-induced damage to DNA is reversible, possibly by defined mechanisms of excision and recombination repair.

Effect of cis -Platinum(II)Diamminodichloride on Wild Type and Deoxyribonucleic Acid Repair-Deficient Mutants of Escherichia coli