Women are More Susceptible Than Men to Oxidative Stress and Chromosome Damage Caused by Polycyclic Aromatic Hydrocarbons Exposure
Women are More Susceptible Than Men to Oxidative Stress and Chromosome Damage Caused by Polycyclic Aromatic Hydrocarbons Exposure
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女性比男性更容易受到多环芳烃暴露引起的氧化应激和染色体损伤
DOI：
10.1002/em.21866
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发表时间：
2014-07-01
影响因子：
2.8
通讯作者：
Wu, Tangchun
中科院分区：
文献类型：
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作者：
Guo, Huan;Huang, Kun;Wu, Tangchun
暴露于环境多环芳烃（PAH）与癌症风险增加有关，但这种关联的性别差异证据有限。本研究的目的是研究多环芳烃的性别差异引起的早期遗传毒性效应，如氧化应激和染色体损伤，这是潜在的致癌性多环芳烃的病因。从一家焦炉厂共招募了478名非吸烟工人（272名男性和206名女性）。我们在工作场所测定了16种环境多环芳烃，并测量了所有受试者的12种尿多环芳烃代谢物（OH-PAH）、血浆苯并[a]芘-r-7、t-8、t-9、c-10-四氢四醇-白蛋白（BPDE-Alb）加合物、尿8-羟基脱氧鸟苷（8-OHdG）和8-异前列腺素-F2α（8-iso-PGF 2 α）的浓度以及淋巴细胞微核率。结果显示，在办公室、焦炉旁、焦炉底部或侧部工作的女性尿8-OHdG、8-iso-PGF 2 α水平及淋巴细胞微核率均显著高于男性（均P <0. 05）。在调整潜在混杂因素和尿中羟苯多环芳烃或血浆中BPDE-Alb加合物后，这些性别差异仍然显著。性别和BPDE-Alb加合物之间存在显著的交互作用，使微核率增加（P交互作用< 0.001）。我们进一步将所有工人按尿中羟苯多环芳烃或血浆BPDE-Alb加合物的三分位数分层，上述性别差异在中位和高暴露组中更为明显（均P < 0.05）。总之，女性比男性更容易受到多环芳烃诱导的氧化应激和染色体损伤，这可能增加了多环芳烃暴露相关肺癌发生性别差异的潜在证据。Environ.摩尔变异体55：472-481，2014.© 2014 Wiley Periodicals，Inc.
Exposure to environmental polycyclic aromatic hydrocarbons (PAHs) has been associated with increased risk of cancer, but evidence for gender differences in this association is limited. The aim of this study was to examine the gender differences in PAHs caused early genotoxic effects such as oxidative stress and chromosome damage, which are potential carcinogenic etiology of PAHs. A total of 478 nonsmoking workers (272 men and 206 women) from a coke oven plant were recruited. We determined 16 environmental PAHs in their workplaces, and measured concentrations of 12 urinary PAH metabolites (OH‐PAHs), plasma benzo[a]pyrene‐r‐7,t‐8,t‐9,c‐10‐tetrahydotetrol‐albumin (BPDE‐Alb) adducts, urinary 8‐hydroxydeoxyguanosine (8‐OHdG) and 8‐iso‐prostaglandin‐F2α (8‐iso‐PGF2α), and micronucleus frequencies in lymphocytes in all subjects. It showed that, women working at the office, adjacent to the coke oven, and on the bottom or side of the coke oven displayed significantly higher levels of urinary 8‐OHdG and 8‐iso‐PGF2α, and lymphocytic micronucleus frequencies compared with men working at above areas, respectively (all P < 0.05). These gender differences remain significant after adjusted for potential confounders and urinary ΣOH‐PAHs or plasma BPDE‐Alb adducts. A significant interaction existed between gender and BPDE‐Alb adducts on increasing micronucleus frequencies (Pinteraction < 0.001). We further stratified all workers by the tertiles of urinary ΣOH‐PAHs or plasma BPDE‐Alb adducts, and the above gender differences were more evident in the median‐ and high‐exposure groups (all P < 0.05). In conclusion, women were more susceptible than men to oxidative stress and chromosome damage induced by PAHs, which may add potential evidence underlying gender differences in PAH exposure‐related lung cacinogenesis. Environ. Mol. Mutagen. 55:472–481, 2014. © 2014 Wiley Periodicals, Inc.