Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats

Abstract

Sulfur dioxide (SO 2) is an air pollutant in densely populated areas as well as in areas polluted by coal-fired power plants, smelters, and sulfuric acid factories. In the present study, male Wistar rats were housed in exposure chambers and treated with 14.00 ± 1.01, 28.00 ± 1.77, and 56.00 ± 3.44 mg/m 3 SO 2for 6 h/day for 7 days, while control rats were exposed to filtered air in the same condition. The mRNA and protein levels of three apoptosis-related genes (p53 and bax are promoters of apoptosis, whereas bcl-2 is apoptotic suppressor) were analyzed in lungs using a real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay and immunohistochemistry method, and caspase-3 activities were detected. The results showed that mRNA levels of p53 and bax were increased in a dose-dependent manner and at the concentrations of 28.00 and 56.00 mg/m 3 SO 2 the increases were significant (for p53: 1.23-fold at 28 mg/m 3 and 1.39-fold at 56 mg/m 3; for bax: 1.77-fold at 28 mg/m 3 and 2.26-fold at 56 mg/m 3, respectively), while mRNA levels of bcl-2 were decreased significantly (0.78-fold at 28 mg/m 3 and 0.73-fold at 56 mg/m 3) in lungs of rats exposed to SO 2. Dose-dependent increase of p53 and bax proteins in the lungs was observed after SO 2 inhalation, while decrease of bcl-2 protein levels was obtained using immunohistochemistry method. Caspase-3 activities were increased in lungs of rats after SO 2 inhalation. These results lead to a conclusion that SO 2 exposure can change the expression of apoptosis-related genes, and it suggests that SO 2 can induce apoptosis in lung of rat and may have relations with some apoptosis-related diseases. Elucidating the expression patterns of those factors after SO 2 inhalation may be critical to our understanding mechanisms of SO 2 toxicity and helpful for the therapeutic intervention.