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PMID: 16449970 Published · ppublish English Journal Article

Effects of hTERT on metal ion-induced genomic instability.

Oncogene ·Vol. 25 ·No. 24 ·2006-06-08 ·Pages 3424-35

Glaviano A, Nayak V, Cabuy E, Baird DM, Yin Z, Newson R, Ladon D, Rubio MA, Slijepcevic P, Lyng F, Mothersill C, Case CP

Abstract

There is currently a great interest in delayed chromosomal and other damaging effects of low-dose exposure to a variety of pollutants which appear collectively to act through induction of stress-response pathways related to oxidative stress and ageing. These have been studied mostly in the radiation field but evidence is accumulating that the mechanisms can also be triggered by chemicals, especially heavy metals. Humans are exposed to metals, including chromium (Cr) (VI) and vanadium (V) (V), from the environment, industry and surgical implants. Thus, the impact of low-dose stress responses may be larger than expected from individual toxicity projections. In this study, a short (24 h) exposure of human fibroblasts to low doses of Cr (VI) and V (V) caused both acute chromosome damage and genomic instability in the progeny of exposed cells for at least 30 days after exposure. Acutely, Cr (VI) caused chromatid breaks without aneuploidy while V (V) caused aneuploidy without chromatid breaks. The longer-term genomic instability was similar but depended on hTERT positivity. In telomerase-negative hTERT- cells, Cr (VI) and V (V) caused a long lasting and transmissible induction of dicentric chromosomes, nucleoplasmic bridges, micronuclei and aneuploidy. There was also a long term and transmissible reduction of clonogenic survival, with an increased beta-galactosidase staining and apoptosis. This instability was not present in telomerase-positive hTERT+ cells. In contrast, in hTERT+ cells the metals caused a persistent induction of tetraploidy, which was not noted in hTERT- cells. The growth and survival of both metal-exposed hTERT+ and hTERT- cells differed if they were cultured at subconfluent levels or plated out as colonies. Genomic instability is considered to be a driving force towards cancer. This study suggests that the type of genomic instability in human cells may depend critically on whether they are telomerase-positive or -negative and that their sensitivities to metals could depend on whether they are clustered or diffuse.

MeSH Terms
Apoptosis Carcinogens/toxicity Cell Survival Chromium/pharmacology Chromosome Aberrations DNA-Binding Proteins/metabolism,physiology Fibroblasts/metabolism Genomic Instability Humans In Situ Hybridization, Fluorescence Ions Micronucleus Tests Telomerase/metabolism,physiology Time Factors Vanadium/pharmacology beta-Galactosidase/metabolism
Chemicals
Carcinogens DNA-Binding Proteins Ions Vanadium Chromium Telomerase beta-Galactosidase
Authors & Affiliations
12 authors, click to expand affiliations / ORCID
Glaviano A
Bristol Implant Research Centre, University of Bristol, Bristol, UK.
Nayak V
Cabuy E
Baird D M
Yin Z
Newson R
Ladon D
Rubio M A
Slijepcevic P
Lyng F
Mothersill C
Case C P
Article Info
Journal
Oncogene
Abbr.
Oncogene
ISSN
0950-9232
Published
2006-06-08
Epub
2006-00-30
Pages
3424-35
Language
English
Region
England
NLM ID
8711562
Subset
IM
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