Use of repair-deficient strains of Escherichia coli and liver microsomes to detect and characterise DNA damage caused by pyrrolizidine alkaloids heliotrine and monocrotaline.
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.
D000818:Animals; D004260:DNA Repair / Q000187:drug effects*; D004926:Escherichia coli / Q000187:drug effects* / Q000378:metabolism; D005838:Genotype; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism*; D008937:Mitomycins / Q000494:pharmacology; D009153:Mutagens; D009154:Mutation; D011763:Pyrrolizidine Alkaloids / Q000494:pharmacology*; D051381:Rats
D008937:Mitomycins; D009153:Mutagens; D011763:Pyrrolizidine Alkaloids; C010178:heliotrine