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Mutagenesis Advance Access originally published online on November 7, 2007
Mutagenesis 2008 23(1):51-56; doi:10.1093/mutage/gem042
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© The Author 2007. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

DNA repair deficiency and acetaldehyde-induced chromosomal alterations in CHO cells

Manuela Mechilli, Angelo Schinoppi, Katarzyna Kobos, Adayapalam T. Natarajan and Fabrizio Palitti*

Department of Agrobiology and Agrochemistry, University of Tuscia, Via S. C. De Lellis snc, I-01100 Viterbo, Italy

Induction of chromosomal aberrations (CAs) and sister chromatid exchanges (SCEs) by acetaldehyde (AA) was evaluated in parental and different DNA repair-deficient Chinese hamster ovary (CHO) cell lines to elucidate the mechanisms involved in the protection against AA-induced chromosome damage. Cell lines employed included the parental (AA8), nucleotide excision repair (UV4, UV5, UV61), base excision repair (EM9), homologous recombination repair (HRR) (irs1SF, 51D1)-deficient and Fanconi-like (KO40) ones. The ranking of different cell lines for sensitivity to induction of CAs by AA was 51D1 > irs1SF > KO40 > UV4 > V33-EM9-AA8 > UV61-UV5 in a descending order. Cells deficient in HRR were most sensitive followed by Fanconi anaemia like (KO40) suggesting these pathways, especially HRR is very important for the repair of AA-induced lesions. These observations also suggest that interstrand cross links are primary biologically relevant DNA lesions induced by AA for induction of CAs. Only marginal differences were found between the cell lines for induction of SCEs. The possible mechanisms involved in AA-induced chromosomal alterations are discussed.

* To whom correspondence should be addressed. Tel: +39 0761 357206; Fax: +39 0761 357242; Email: palitti{at}unitus.it

Received on June 18, 2007; revised on September 24, 2007; accepted on September 24, 2007.


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