Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats.
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.
Bai
Juli
J
Institute of Environmental Medicine and Toxicology, Shanxi University, Taiyuan 030006, China. baijuli@sxu.edu.cn
Meng
Ziqiang
Z
D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics*; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D019254:Genes, bcl-2 / Q000187:drug effects; D016158:Genes, p53 / Q000187:drug effects; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000378:metabolism; D007150:Immunohistochemistry; D008168:Lung / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013458:Sulfur Dioxide / Q000633:toxicity*; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; D013458:Sulfur Dioxide; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases