Influence of different concentrations of ozone on the alteration of mitochondrial DNA copy numbers in human peripheral blood.

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.