Abstract
E. coli WP2 and its repair-deficient derivatives were treated with the pyrrolizidine alkaloids, heliotrine and monocrotaline in the presence of a liver microsomal fraction. The doubly repair-deficient strains WP100 uvrA recA and CM611 uvrA exrA showed considerable killing. The singly repair-deficient strains WP2 uvrA, CM561 exrA and CM571 recA showed slight killing. In strains WP2 and WP2 uvrA induced reversion to Trp + was not detected with either monocrotaline or mitomycin C. These results are entirely consistent with liver activation converting pyrrolizidine alkaloids into bifunctional alkylating agents.
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