Defective Repair of Tryptophan Pyrolysate (Trp P-1 and Trp P-2) and Aflatoxin BL Damage in Xeroderma Pigmentosum Cells

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Optimally activated aflatoxin Bi (AFB1), 3-amino-1, 4-dimethyl- and 3-amino-1-methyl5H-pyrido[4, 3-b]indoles (Trp P-1 and Trp P-2) exerted more lethal effects on xeroderma pigmentosum (XP) complementation group G cells than on normal human ells. XP group G cells exhibited deficiency in unscheduled DNA synthesis and in accumulation of arabinofuranosyl cytosine/hydroxyurea-induced single strand breaks after treatment with the three agents. Thus, Trp P-1 or Trp P-2 damage can be repaired mainly by nucleotide excision repair, as found with AFB1 damage. Activated AFB1 induced more sister chromatid exchanges (SCEs) in XP group G cells than in normal cells, while such a differential response to SCE was not observed with activated Trp P-1 and Trp P-2. Mycotoxin aflatoxin Bi (AFB#) and tryptophan pyrolysis principles Trp P-1 and Trp P-2 are not only mutagenic to bacterial1-4) and mammalian5-7 cells, when metabolically activated with liver microsomal enzymes, but also oncogenic to mammals. 7-9)
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