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In the present study, male Wistar rats were housed in exposure chambers and treated with 14.00 \u00b1 1.01, 28.00 \u00b1 1.77 and 56.00 \u00b1 3.44 mg m<jats:sup>\u22123<\/jats:sup>SO<jats:sub>2<\/jats:sub>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\u2010oncogenes (c\u2010fos, c\u2010jun, c\u2010myc, and Ki\u2010ras) and tumor suppressor genes (p53, Rb, and p16) were analyzed in lungs using a real\u2010time reverse transcription\u2010polymerase chain reaction (real\u2010time RT\u2010PCR) assay and Western blot analysis. The results showed that mRNA and protein levels of c\u2010fos, c\u2010jun, c\u2010myc, Ki\u2010ras, and p53 in lungs were increased in a dose\u2010dependent manner, while mRNA and protein levels of Rb and p16 were decreased in lungs of rats after SO<jats:sub>2<\/jats:sub>inhalation. These results lead to a conclusion that SO<jats:sub>2<\/jats:sub>exposure could activate expressions of proto\u2010oncogenes and suppress expressions of tumor suppressor genes, which might relate to the molecular mechanism of cocarcinogenic properties and potential carcinogenic effects of SO<jats:sub>2<\/jats:sub>. 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. \u00a9 2009 Wiley Periodicals, Inc. 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