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 m-3 SO2 for 6 h/day for 7 days, while control group was exposed to filtered air in the same condition. The mRNA and protein levels of proto-oncogenes (c-fos, c-jun, c-myc, and Ki-ras) and tumor suppressor genes (p53, Rb, and p16) were analyzed in lungs using a real-time reverse transcription-polymerase chain reaction (realtime RT-PCR) assay and Western blot analysis. The results showed that mRNA and protein levels of c-fos, c-jun, c-myc, Ki-ras, and p53 in lungs were increased in a dose-dependent manner, while mRNA and protein levels of Rb and p16 were decreased in lungs of rats after SO2 inhalation. These results lead to a conclusion that SO2 exposure could activate expressions of proto-oncogenes and suppress expressions of tumor suppressor genes, which might relate to the molecular mechanism of cocarcinogenic properties and potential carcinogenic effects of SO2. According to previous studies, the results also indicated that promoter genes of apoptosis and tumor suppressor genes could produce apoptotic signals to antagonize the growth signals that arise from oncogenes. Understanding its molecular controls will benefit development of treatments for many diseases.
- Sulfur dioxide
- Tumor suppressor gene
ASJC Scopus subject areas
- Health, Toxicology and Mutagenesis
- Management, Monitoring, Policy and Law