Evaluation of genome damage in subjects occupationally exposed to possible carcinogens

被引:2
|
作者
Zeljezic, Davor [1 ]
Mladinic, Marin [1 ]
Kopjar, Nevenka [1 ]
Radulovic, Azra Hursidic
机构
[1] Inst Med Res & Occupat Hlth, Div Mutagenesis, Ksaverska 2, Zagreb 10000, Croatia
关键词
Comet assay; micronucleus assay; comet-FISH; TP; 53; occupational exposure; PERIPHERAL-BLOOD LYMPHOCYTES; IN-SITU HYBRIDIZATION; DNA-DAMAGE; ETHYLENE-OXIDE; CHROMOSOMAL-ABNORMALITIES; CYTOME ASSAY; COMET ASSAY; CANCER; CELLS; GENOTOXICITY;
D O I
10.1177/0748233714568478
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
In occupational exposures, populations are simultaneously exposed to a mixture of chemicals. We aimed to evaluate DNA damage due to possible carcinogen exposure (phenylhydrazine, ethylene oxide, dichloromethane, and 1,2-dichloroethane) in lymphocytes of pharmaceutical industry workers from the same production line. Population comprised 16 subjects (9 females and 7 males) who were exposed to multiple chemicals for 8 months. Genome damage was assessed using alkaline comet assay, micronucleus assay, and comet assay coupled with fluorescent in situ hybridization (comet-FISH). After 8 months of exposure, the issue of irregular use of all available personal protective equipment (PPE) came into light. To decrease the risk of exposure, strict use of PPE was enforced. After 8 months of strict PPE use, micronuclei frequency and comet assay parameters in lymphocytes of pharmaceutical workers significantly decreased compared with prior period of irregular PPE use. Comet-FISH results indicated a significant shift in distribution of signals for the TP 53 gene toward a more frequent occurrence in the comet tail. Prolonged exposure to possible carcinogens may hinder DNA repair mechanisms and affect structural integrity of TP 53. Two indicators of loss of TP 53 gene integrity have risen, namely, TP 53 fragmentation rate in lymphocytes with persistently elevated primary damage and incidence of TP 53 deletions in undamaged lymphocytes.
引用
收藏
页码:1570 / 1580
页数:11
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