The response of Xeroderma pigmentosum cells and controls to the activated mycotoxins, aflatoxins and sterigmatocystin.
The activation of the mycotoxins aflatoxin B1, G1, B2, G2, aflatoxicol and sterigmatocystin by 9S fraction, microsomal preparation (105,000 times g) and supernatant (105,000 times g) of livers of several species was examined. DNA repair synthesis, chromosome aberrations and clone forming capacity were used as endpoints. Cultured fibroblasts of normal persons and DNA repair deficient Xeroderma pigmentosum patients were employed as test subjects. The activation mixtures significantly increase the chromosome breaking function, lethality and DNA damaging effect (measured as DNA repair synthesis) of aflatoxin B1, G1, aflatoxicol ans sterigmatocystin. The DNA repair-deficient XP cells respond to the activated mycotoxins with a low level of unscheduled 3HTdR incorporation as compared to that of control cells, but show a highly elevated sensitivity to the chromosome-damaging and lethal effect of aflatoxin B1 and sterigmatocystin.
D000348:Aflatoxins / Q000378:metabolism / Q000494:pharmacology* / Q000633:toxicity; D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D002869:Chromosome Aberrations; D002999:Clone Cells; D006224:Cricetinae; D004247:DNA / Q000096:biosynthesis; D004260:DNA Repair / Q000187:drug effects*; D004372:Ducks; D005347:Fibroblasts / Q000187:drug effects / Q000648:ultrastructure; D006801:Humans; D007668:Kidney / Q000378:metabolism; D051379:Mice; D008862:Microsomes, Liver / Q000378:metabolism*; D009153:Mutagens; D009928:Organ Specificity; D011817:Rabbits; D013241:Sterigmatocystin / Q000378:metabolism / Q000494:pharmacology* / Q000633:toxicity; D014337:Trout; D014966:Xanthenes / Q000494:pharmacology*; D014983:Xeroderma Pigmentosum / Q000235:genetics / Q000378:metabolism / Q000473:pathology
D000348:Aflatoxins; D009153:Mutagens; D014966:Xanthenes; D013241:Sterigmatocystin; D004247:DNA