Dibenzo[a,h]anthracene and Benzo[a]anthracene increase oxidative stress in human bronchial epithelial cells

• Investigating the cell damage caused by PAHs containing anthracene at low concentration on human bronchial epithelial cells and the abnormal expression of oxidative stress markers. • Filling a gap in toxicological studies of PAHs containing "anthracene" in low concentrations at environmental concentrations. • Providing theoretical and experimental basis for the prevention and treatment of human bronchial epithelial cell injury caused by PAHs containing low concentration of "anthracene". Dibenzo[a,h]anthracene (DahA) and Benzo[a]anthracene (BaA), as the main components in gasoline, diesel, and coal combustion products, dominate air pollution in northern China and pose a serious threat to human health. In this study, different concentrations of DahA and BaA were used to intervene in human bronchial epithelial cells. Cell viability was determined by using the thiazolyl blue assay; Intracellular reactive oxygen species (ROS) levels were measured using fluorescence microscopy and flow cytometry; The oxidative damage effect was evaluated by measuring the production of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in cells; Finally, real-time fluorescence quantitative reverse transcription polymerase Chain reaction and protein immunoblotting were used to detect the changes in the expression of copper/zinc superoxide dismutase (SOD1) and manganese superoxide dismutase (SOD2) at the gene and protein levels. The results showed that the cell survival rate decreased with increasing concentration after 24 h of DahA and BaA intervention. Compared with the control group, the average fluorescence intensity of ROS increased at 100, 1000, and 10,000 pg/ml, MDA levels increased, and SOD levels decreased. At the gene and protein levels, the mRNA and protein expression of SOD1 and SOD2 increased at 1000 pg/ml and 10,000 pg/ml, respectively. In summary, DahA and BaA have toxic effects on human bronchial epithelial cells after 24 h of intervention and can cause changes in oxidative stress indicators, indicating the occurrence of oxidative stress damage. Oxidative stress damage to human bronchial epithelial cells may be the main mechanism of PAHs on respiratory system damage.