Bin Ping, Shen Meili, Li Haibin, Sun Xin, Niu Yong, Meng Tao, Yu Tao, Zhang Xiao, Dai Yufei, Gao Weimin, Gu Guizhen, Yu Shanfa, Zheng Yuxin
a Key Laboratory of Chemical Safety and Health , National Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention , Beijing , China ;
b Department of Environmental Toxicology , The Institute of Environmental and Human Health, Texas Tech University , Lubbock , TX , USA ;
Free Radic Res. 2016 Aug;50(8):820-30. doi: 10.1080/10715762.2016.1178738. Epub 2016 May 12.
Diesel engine exhaust (DEE) was found to induce lipid peroxidation (LPO) in animal exposure studies. LPO is a class of oxidative stress and can be reflected by detecting the levels of its production, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), and etheno-DNA adducts including 1,N(6)-etheno-2'-deoxyadenosine (ɛdA) and 3,N(4)-etheno-2'-deoxycytidine (ɛdC). However, the impact of DEE exposure on LPO has not been explored in humans. In this study, we evaluated urinary MDA, 4-HNE, ɛdA, and ɛdC levels as biomarkers of LPO among 108 workers with exclusive exposure to DEE and 109 non-DEE-exposed workers. Results showed that increased levels of urinary MDA and ɛdA were observed in subjects occupationally exposed to DEE before and after age, body mass index (BMI), smoking status, and alcohol use were adjusted (all p < 0.001). There was a statistically significant relationship between the internal exposure dose (urinary ΣOH-PAHs) and MDA, 4-HNE, and ɛdA (all p < 0.001). Furthermore, significant increased relations between urinary etheno-DNA adduct and MDA, 4-HNE were observed (all p < 0.05). The findings of this study suggested that the level of LPO products (MDA and ɛdA) was increased in DEE-exposed workers, and urinary MDA and ɛdA might be feasible biomarkers for DEE exposure. LPO induced DNA damage might be involved and further motivated the genomic instability could be one of the pathogeneses of cancer induced by DEE-exposure. However, additional investigations should be performed to understand these observations.
在动物暴露研究中发现，柴油机尾气（DEE）可诱导脂质过氧化（LPO）。LPO是一类氧化应激反应，可通过检测其产物水平来反映，如丙二醛（MDA）、4-羟基壬烯醛（4-HNE）以及包括1,N(6)-乙烯基-2'-脱氧腺苷（ɛdA）和3,N(4)-乙烯基-2'-脱氧胞苷（ɛdC）在内的乙烯基-DNA加合物。然而，DEE暴露对LPO的影响尚未在人类中进行研究。在本研究中，我们评估了108名仅暴露于DEE的工人和109名未暴露于DEE的工人尿液中MDA、4-HNE、ɛdA和ɛdC水平，将其作为LPO的生物标志物。结果显示，在对年龄、体重指数（BMI）、吸烟状况和饮酒情况进行调整后，职业暴露于DEE的受试者尿液中MDA和ɛdA水平升高（所有p < 0.001）。内暴露剂量（尿中ΣOH-PAHs）与MDA、4-HNE和ɛdA之间存在统计学显著关系（所有p < 0.001）。此外，观察到尿中乙烯基-DNA加合物与MDA、4-HNE之间存在显著的增加关系（所有p < 0.05）。本研究结果表明，暴露于DEE的工人中LPO产物（MDA和ɛdA）水平升高，尿中MDA和ɛdA可能是DEE暴露的可行生物标志物。LPO诱导的DNA损伤可能参与其中，进一步引发的基因组不稳定可能是DEE暴露诱发癌症的发病机制之一。然而，需要进行更多研究以了解这些观察结果。
