Li Zhigang, Su Qiaoqiao, Xu Rongrong, Peng Jianhao, Zhu Xiaojing, Wei Yongjie
State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing, China.
State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing, China; Center for Global Health, School of Public Health, Nanjing Medical University, China.
Sci Total Environ. 2023 May 15;873:162282. doi: 10.1016/j.scitotenv.2023.162282. Epub 2023 Feb 16.
By now, O pollution has become a main environmental problem. O is a prevalent risk factor for many diseases, but the regulatory factors linking O and diseases remain ambiguous. Mitochondrial DNA (mtDNA) is the genetic material in mitochondria, which plays a key role in the production of respiratory ATP. Due to a lack of histone protection, mtDNA is easily damaged by ROS, and O is an important source to stimulate the production of endogenous ROS in vivo. Therefore, we logically speculate that O exposure can alter mtDNA copy number by the induction of ROS. In the present study, we performed a panel study of 65 MSc students at the Chinese research academy of environmental sciences (CRAES) with 3 rounds of follow-up visits from August 2021 to January 2022. We examined the mtDNA copy numbers in the peripheral blood of subjects using quantitative polymerase chain reaction. Linear mixed-effect (LME) model and stratified analysis were used to investigate the association between O exposure and mtDNA copy numbers. We found a dynamic process of the association between the concentration of O exposure and the mtDNA copy number in the peripheral blood. The lower concentration of O exposure did not affect the mtDNA copy number. As the concentration of O exposure increased, the mtDNA copy number also increased. While, when O exposure reached a certain concentration, a decrease in mtDNA copy number was found. This correlation between the concentration of O and the mtDNA copy number could be ascribed to the severity of cellular damage induced by O exposure. Our results provide a new perspective for the discovery of a biomarker of O exposure and health response, as well as for the prevention and treatment of adverse health effects caused by different concentrations of O.
到目前为止，臭氧污染已成为一个主要的环境问题。臭氧是许多疾病的普遍风险因素，但将臭氧与疾病联系起来的调节因素仍不明确。线粒体DNA（mtDNA）是线粒体中的遗传物质，在呼吸性ATP的产生中起关键作用。由于缺乏组蛋白保护，mtDNA很容易被活性氧（ROS）损伤，而臭氧是体内刺激内源性ROS产生的重要来源。因此，我们合理推测，臭氧暴露可通过诱导ROS来改变mtDNA拷贝数。在本研究中，我们对中国环境科学研究院的65名硕士研究生进行了一项队列研究，从2021年8月至2022年1月进行了3轮随访。我们使用定量聚合酶链反应检测了受试者外周血中的mtDNA拷贝数。采用线性混合效应（LME）模型和分层分析来研究臭氧暴露与mtDNA拷贝数之间的关联。我们发现臭氧暴露浓度与外周血mtDNA拷贝数之间存在动态关联过程。较低浓度的臭氧暴露不影响mtDNA拷贝数。随着臭氧暴露浓度的增加，mtDNA拷贝数也增加。然而，当臭氧暴露达到一定浓度时，发现mtDNA拷贝数下降。臭氧浓度与mtDNA拷贝数之间的这种相关性可归因于臭氧暴露诱导的细胞损伤的严重程度。我们的研究结果为发现臭氧暴露和健康反应的生物标志物以及预防和治疗不同浓度臭氧引起的不良健康影响提供了新的视角。
