Expression of apoptosis-related genes in livers from rats exposed to sulfur dioxide.
Sulfur dioxide (SO2) is a ubiquitous air pollutant that is present in low concentrations in the urban air, and in higher concentrations in the working environment. 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 were promoters of apoptosis, whereas bcl-2 was apoptotic suppressor) were analyzed in livers using a real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay and immunohistochemistry method. 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/m3SO2 the increases were significant (for p53: 1.30-fold at 28 mg/m3 and 3.43-fold at 56 mg/m3, for bax: 1.63-fold at 28 mg/m3 and 2.17-fold at 56 mg/m3, respectively), while mRNA levels of bcl-2 were decreased significantly (0.63-fold at 28 mg/m3 and 0.45-fold at 56 mg/m3) in livers of rats exposed to SO2. Dose-dependent increases of p53 and bax proteins in the livers were observed after SO2 inhalation, while decrease of bcl-2 protein levels was obtained using immunohistochemistry method. These results lead to a conclusion that SO2 exposure could change the expression of apoptosis-related genes, and it suggests that SO2 can induce apoptosis in liver of rat and may have relations with some apoptosis-related diseases. It is critical for our understanding of the mechanisms of SO2 toxicity and helpful for the therapeutic intervention to elucidate the expression pattern of those factors involved in apoptosis signaling pathway after SO2 inhalation.
Bai
Juli
J
Institute of Environmental Medicine and Toxicology, Shanxi University, Taiyuan 030006, China. baijuli@sxu.edu.cn
Meng
Ziqiang
Z
D000393:Air Pollutants / Q000378:metabolism / Q000633:toxicity*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics*; D004305:Dose-Response Relationship, Drug; D005784:Gene Amplification / Q000187:drug effects; D015870:Gene Expression / Q000187:drug effects*; D019254:Genes, bcl-2 / Q000187:drug effects / Q000235:genetics; D016158:Genes, p53 / Q000187:drug effects / Q000235:genetics; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000235:genetics / Q000378:metabolism; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D007150:Immunohistochemistry; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D016133:Polymerase Chain Reaction / Q000379:methods; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013458:Sulfur Dioxide / Q000378:metabolism / Q000633:toxicity*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000187:drug effects / Q000235:genetics / Q000378:metabolism
D000393:Air Pollutants; C494828:Bax protein, rat; D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D013458:Sulfur Dioxide; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases