Literature DB >> 25381312

Nucleoplasmic bridges and acrocentric chromosome associations as early markers of exposure to low levels of ionising radiation in occupationally exposed hospital workers.

Fabio Caradonna1.   

Abstract

Ionising radiation, with the contribution of telomere shortening, induces DNA double-strand breaks that result in chromosome end fusion, nucleoplasmic bridges (NPBs) and chromosome aberrations (ChAbs) as well as dicentric chromosomes. In order to investigate the chromosomal damage induced by occupational ionising radiation at low exposure levels, and to find early markers of health hazard, peripheral lymphocytes of occupationally exposed hospital workers were cytogenetically analysed. Results showed a significant difference in the frequency of ChAbs in exposed subjects relative to controls. A significant number of NPBs between nuclei of binucleated cultured lymphocytes from exposed subjects were also observed, as well as a consistent amount of acrocentric chromosomes with associations of their short arms. Excluding confounding factors, the frequencies of all these three biological endpoints differed significantly in exposed subjects from those in controls. Because the absence of telomeres and/or their short length could be a common root for both the findings, we utilised fluorescence in situ hybridisation technique with telomeric repeat as probe to demonstrate that, in exposed subjects, chromatin of short arms of involved acrocentric chromosomes did not exhibit a telomeric shortening but appeared strongly decondensed. This finding suggests that NPBs and telomeric acrocentric association should be regarded as early markers of exposure to low levels of ionising radiation and their increase should be seen as an early warning for the health of the involved workers.
© The Author 2014. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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Year:  2014        PMID: 25381312     DOI: 10.1093/mutage/geu068

Source DB:  PubMed          Journal:  Mutagenesis        ISSN: 0267-8357            Impact factor:   3.000


  5 in total

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