Author(s): Bai J, Meng Z
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Abstract Sulfur dioxide (SO2) 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/m3 SO2 for 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/m3 SO2 the increases were significant (for p53: 1.23-fold at 28 mg/m3 and 1.39-fold at 56 mg/m3; for bax: 1.77-fold at 28 mg/m3 and 2.26-fold at 56 mg/m3, respectively), while mRNA levels of bcl-2 were decreased significantly (0.78-fold at 28 mg/m3 and 0.73-fold at 56 mg/m3) in lungs of rats exposed to SO2. Dose-dependent increase of p53 and bax proteins in the lungs was observed after SO2 inhalation, while decrease of bcl-2 protein levels was obtained using immunohistochemistry method. Caspase-3 activities were increased in lungs of rats after SO2 inhalation. These results lead to a conclusion that SO2 exposure can change the expression of apoptosis-related genes, and it suggests that SO2 can induce apoptosis in lung of rat and may have relations with some apoptosis-related diseases. Elucidating the expression patterns of those factors after SO2 inhalation may be critical to our understanding mechanisms of SO2 toxicity and helpful for the therapeutic intervention.
This article was published in Regul Toxicol Pharmacol
and referenced in Journal of Environmental & Analytical Toxicology