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Mutagenesis Advance Access originally published online on January 27, 2008
Mutagenesis 2008 23(2):101-109; doi:10.1093/mutage/gem049
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© The Author 2008. 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.

Pre-irradiation exposure of peripheral blood lymphocytes to glutaraldehyde induces radiosensitization by increasing the initial yield of radiation-induced chromosomal aberrations

Vasiliki I. Hatzi, Georgia I. Terzoudi*, Vasilios Makropoulos1, Constantinos Maravelias2 and Gabriel E. Pantelias

Health Physics Laboratory, National Centre for Scientific Research "Demokritos," 15310 Agia Paraskevi, Athens, Greece 1Department of Occupational Hygiene, National School of Public Health, Athens, Greece & Hellenic Institute for Occupational Health and Safety ELINYAE, Athens, Greece 2Department of Forensic Medicine and Toxicology, Medical School, University of Athens, Greece

Glutaraldehyde (GA) is a high production volume chemical that is very reactive with a wide spectrum of medical, scientific and industrial applications. Since human exposure in anthropogenic and occupational environment occurs frequently, GA has been extensively tested for genotoxic activity in vitro and in vivo. However, there are conflicting results in the literature and there is a lack of information concerning the combined effects of exposure to both GA and ionizing radiation in human cells. In the present study, the results obtained using conventional cytogenetic analysis do not suggest a statistically significant clastogenic or genotoxic activity of GA when concentrations in the range of 10–6 to 10–2 mM were applied. However, a 24-h pre-irradiation exposure of human peripheral blood lymphocytes (PBLs) to non-genotoxic doses of GA showed a statistically significant (P > 0.05) increase in chromosomal radiosensitivity. The observed increase may be an effect of GA-induced alterations in the cell-cycle and feedback control mechanisms during the cell-cycle transition points or it may be a consequence of an effect of GA either on the DNA repair capacity of the cells after irradiation or on the initial induction of radiation-induced chromosomal damage. To elucidate the mechanism underlying the obtained radiosensitization, conventional cytogenetics, the G2 chromosomal radiosensitivity assay and premature chromosome condensation methodologies were applied. The results support the hypothesis that pre-irradiation exposure of PBLs to GA induces radiosensitization by increasing the initial yield of chromosomal aberrations following irradiation.

* To whom correspondence should be addressed. Tel: +30 210 6503865/210 6529615; Fax: +30 210 6534710; Email: georgia{at}ipta.demokritos.gr

Received on October 12, 2007; revised on November 23, 2007; accepted on November 26, 2007.


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