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Arsenic[III] and heavy metal ions induce intrachromosomal homologous recombination in the hprt gene of V79 Chinese hamster cells
Author(s) -
Helleday Thomas,
Nilsson Robert,
Jenssen Dag
Publication year - 2000
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/(sici)1098-2280(2000)35:2<114::aid-em6>3.0.co;2-q
Subject(s) - homologous recombination , chinese hamster , microbiology and biotechnology , recombination , non homologous end joining , mitotic crossover , biology , genetic recombination , flp frt recombination , chinese hamster ovary cell , chromatid , dna , genetics , gene conversion , gene , dna repair , homologous chromosome , non allelic homologous recombination , chemistry , cell culture , chromosome
In the present study the carcinogenic metal ions Cd[II], Co[II], Cr[VI], Ni[II], and Pb[II], as well as As[III], were examined for their ability to induce intrachromosomal homologous and nonhomologous recombination in the hprt gene of two V79 Chinese hamster cell lines, SPD8 and Sp5, respectively. With the exception of Pb[II], all of these ions enhanced homologous recombination, the order of potency being Cr>Cd>As>Co>Ni. In contrast, Cr[VI] was the only ion to enhance recombination of the nonhomologous type. In order to obtain additional information on the mechanism of recombination in the SPD8 cell line, individual clones exhibiting metal‐induced recombination were isolated, and the sequence of their hprt gene determined. These findings confirmed that all recombinogenic events in this cell line were of the homologous type, involving predominantly a chromatid exchange mechanism. The mechanisms underlying the recombination induced by these ions are discussed in relationship to their genotoxicity, as well as to DNA repair and replication. Induced recombination may constitute a novel mechanism for induction of neoplastic disease. Environ. Mol. Mutagen. 35:114‐122, 2000 © 2000 Wiley‐Liss, Inc.