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

Abstract

Optimally activated aflatoxin B1 (AFB1), 3-amino-l, 4-dimethyl and 3-amino-l-methyl-5H-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.