Cebulska-Wasilewska Antonina, Pawłyk Igor, Panek Agnieszka, Wiecheć Anna, Kalina Ivan, Popov Todor, Georgieva Tzveta, Farmer Peter B
Department of Radiation and Environmental Biology, The Henryk Niewodniczański Institute of Nuclear Physics PAN, Radzikowskiego 152, 31-342 Kraków, Poland.
Mutat Res. 2007 Jul 1;620(1-2):145-54. doi: 10.1016/j.mrfmmm.2007.03.004. Epub 2007 Mar 12.
The aim of this study was to investigate a possible influence of occupational exposure to carcinogenic environmental polycyclic aromatic hydrocarbons (c-PAHs) on cellular susceptibility to the induction of the DNA damage. Monitoring was performed and blood samples were collected from two groups of male subjects: occupationally exposed and matched controls. The group exposed to c-PAHs (average age of 35.1 years) consisted of 52 policemen from Kosice and 26 policemen and 25 bus drivers (51 altogether) from Sofia. The control group (average age of 36.4 years) consisted of 54 unexposed subjects from Kosice and 24 from Sofia. In the investigated groups 52.5% of exposed subjects and 45.3% of control were current smokers. A challenging dose of X-rays (3Gy) and an alkaline version of the single cell gel electrophoresis (SCGE) assay, known as Comet assay, were used to evaluate levels of induced DNA damage and repair kinetics in isolated human blood lymphocytes. DNA damage detected in lymphocytes prior to or after irradiation did not differ significantly between exposed and unexposed subjects. A significant decrease in repair efficiency due to exposure to PAHs was observed in the exposed individuals from Kosice and Sofia, when analysed separately or together. A negative influence of tobacco smoking on the efficiency of DNA repair was observed. Statistically significant differences were found between subgroups stratified according to education level in Sofia: the half times for DNA repair declined with the increasing level of education. These results confirm that environmental exposure to c-PAHs can alter the ability of blood lymphocytes to repair DNA damage and, as a result could potentially lead to effects that are hazardous to human health.
本研究的目的是调查职业性接触致癌环境多环芳烃（c-PAHs）对细胞DNA损伤诱导易感性的可能影响。对两组男性受试者进行了监测并采集了血样：职业暴露组和匹配的对照组。接触c-PAHs的组（平均年龄35.1岁）包括来自科希策的52名警察以及来自索非亚的26名警察和25名公交车司机（共51人）。对照组（平均年龄36.4岁）包括来自科希策的54名未接触者和来自索非亚的24名未接触者。在被调查的组中，52.5%的暴露受试者和45.3%的对照受试者为当前吸烟者。使用具有挑战性的X射线剂量（3Gy）和碱性单细胞凝胶电泳（SCGE）试验（即彗星试验）来评估分离出的人血淋巴细胞中诱导的DNA损伤水平和修复动力学。暴露组和未暴露组受试者在照射前或照射后淋巴细胞中检测到的DNA损伤没有显著差异。单独或合并分析时，在来自科希策和索非亚的暴露个体中观察到由于接触多环芳烃导致修复效率显著降低。观察到吸烟对DNA修复效率有负面影响。在根据索非亚的教育水平分层的亚组之间发现了统计学上的显著差异：DNA修复的半衰期随着教育水平的提高而下降。这些结果证实，环境接触c-PAHs可改变血淋巴细胞修复DNA损伤的能力，因此可能潜在地导致对人类健康有害的影响。
