Ecevit, HasretUrhan-Kucuk, MeralUluca, HalukTap, DuyguArpaci, Abdullah2024-09-182024-09-1820210095-45271934-9440https://doi.org/10.3103/S0095452721030026https://hdl.handle.net/20.500.12483/7864Oxidative stress is an important pathophysiological factor in chronic respiratory diseases. Our study aimed at elucidating through which pathway oxidative stress-mediated apoptosis occurs at the gene expression level under oxidative stress in the human bronchial epithelial cell line BEAS-2B. Suitable doses and time period were detected by exposing BEAS-2B cells to hydrogen peroxide (H2O2) at different doses and time periods, and the oxidative-damaged cell culture model was designed. The treatment and control groups were compared in terms of gene expression levels determined by Quantitative Real Time Polymerase Chain Reaction. The oxidative-damaged cell model was confirmed by the spectrophotometric measurement of malondialdehyde and catalase activity (p < 0.05). Caspase-3, caspase-9, bax, and bak gene expression levels increased significantly in the treatment groups compared to the control group (p < 0.05). There were not any significant differences between the groups in terms of caspase-8, Bcl-2, and bik (p > 0.05). p53 and p21 gene expression levels were found to be significantly higher in the treatment groups (p < 0.05). H2O2-induced oxidative stress, induced apoptosis through the intrinsic pathway at gene expression level in the bronchial epithelial BEAS-2B cells was observed.eninfo:eu-repo/semantics/closedAccessapoptosisBEAS-2Bcell proliferationoxidative stressreactive oxygen speciesArticle55328328910.3103/S00954527210300262-s2.0-85107134866Q3WOS:000657840200009Q4