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Carcinogenesis Advance Access published online on November 21, 2003
Carcinogenesis, doi:10.1093/carcin/bgh029
© 2003 by Oxford University Press
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© 2003 Oxford University Press

CARCINOGENESIS

Arsenic-induced DNA hypomethylation affects chromosomal instability in mammalian cells

Giulia Sciandrello 1*, Fabio Caradonna 1, Maurizio Mauro 1, and Giusi Barbata 1

1 Dipartimento di Biologia Cellulare e dello Sviluppo "A. Monroy", Università di Palermo, Viale delle Scienze, Parco d'Orleans, 90128 Palermo, Italy

* Corresponding author. E-mail: giscian{at}unipa.it.

Received 28 March 2003 ; revised 10 November 2003 ; accepted 12 November 2003

Abstract

Early genetic instability induced in dividing V79-Cl3 Chinese hamster cells by inorganic arsenic, as demonstrated in our previous investigation, was evidenced by aneuploidy and nuclear abnormalities, but not by chromosomal rearrangements. Here we report the results of cytogenetic and morphological analyses performed on the progeny of cells dividing at the end of SA-treatment after they had been expanded through 120 generations (ASO cells) and then cloned. The acquired genetic instability persisted and was increased by highly instable chromosomal rearrangements, namely dicentric chromosomes and telomeric associations, which were not seen following acute exposure. A peculiar finding was the preferential involvement of a particular chromosome in dicentric rearrangements observed in some isolated ASO clones. Interestingly, by immunostaining with anti-5-methylcytosine antibodies the genome-wide DNA hypomethylation, induced by arsenic immediately after the acute treatment, was found to affect those ASO clones characterized by aneuploidy and chromosomal rearrangements. These findings demonstrate that short-term exposure to arsenic has long-term effects and suggest that genomewide DNA hypomethylation enhances genetic instability.


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