Differences in cellular and molecular processes in exposure to PM and O.

Epidemiological and toxicological studies have shown that PM and O could pose significant risks to human health, such as an increased incidence of respiratory and cardiovascular diseases. Usually, the adverse health outcomes induced by PM and O exposure are similar. However, PM and O have distinct physical and chemical properties, with PM being a solid-liquid mixture and O being a strongly oxidizing gaseous pollutant. Therefore, we speculated that there are some differences in biological processes induced by PM and O exposure. In the present study, we investigated the differences induced by PM and O exposure from the perspective of cellular and molecular processes. Firstly, the pulmonary epithelial cells (BEAS-2B) were exposed to different concentrations of PM or O at different durations. Then, we chose experimental models with the concentrations and duration at which the cell survival rate was 50 % after exposure to PM and O, which were 100 μg/mL for 24 h for PM, and 200 ppb for 4 h for O. Our findings indicate that PM infiltrates cells via endocytosis without causing significant damage to cell membranes, while O induces lipid peroxidation at the cell surface. Moreover, the detection of mitochondrial function showed that the content of ATP was significantly reduced after exposure to both PM and O. However, we found a significant difference in mtDNA copy number. PM exposure increased the mtDNA copy number by up-regulating the expression of fission genes (Fis1, Mff, Dnm1). O exposure decreased it by up-regulating the expression of fusion gene (Mfn1, Mfn2) and down-regulating the expression of fission gene (Fis1, Dnm1). These results indicate that although both PM and O exposure induced almost exactly similar adverse health outcomes, significant differences do exist in cellular and molecular processes.