DNA repair deficiency and BPDE-induced chromosomal alterations in CHO cells.
The induction of chromosomal aberrations and sister chromatid exchanges by BPDE was evaluated in parental and different DNA repair deficient Chinese hamster ovary cell lines in order to elucidate the mechanisms involved in their induction. These included the parental line (AA8), nucleotide excision repair (UV4, UV5, UV61), base excision repair (EM9), homologous recombination repair (Irs1SF) and non-homologous end joining (V3-3) deficient ones. The ranking of different cell lines for BPDE-induced chromosome aberrations was: UV4, Irs1SF, UV5, UV 61, EM9, V3-3, and AA8 in a descending order. Cells deficient in NER and HRR were found to be very sensitive, indicating the importance of these pathways in the repair of lesions induced by BPDE. For induction of SCEs, HRR and BER deficient cells were refractory, whereas the other cell lines responded with a dose-dependent increase. The possible mechanisms involved in BPDE-induced chromosomal alterations are discussed.
Meschini
Roberta
R
Department of Agrobiology and Agrochemistry, University of Tuscia, Via San Camillo de Lellis, 01100, Viterbo, Italy.
Marotta
Edvige
E
Berni
Andrea
A
Filippi
Silvia
S
Fiore
Mario
M
Mancinelli
Pierluigi
P
Natarajan
Adayapalam T
AT
Palitti
Fabrizio
F
D015123:7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide / Q000633:toxicity*; D000818:Animals; D016466:CHO Cells; D002869:Chromosome Aberrations; D006224:Cricetinae; D003412:Cricetulus; D004260:DNA Repair; D009153:Mutagens / Q000633:toxicity*; D012854:Sister Chromatid Exchange
D009153:Mutagens; D015123:7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide