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Effect of sulfur dioxide on expression of proto‐oncogenes and tumor suppressor genes from rats
Author(s) -
Bai Juli,
Meng Ziqiang
Publication year - 2010
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.20495
Subject(s) - suppressor , carcinogen , gene , western blot , tumor suppressor gene , messenger rna , apoptosis , e2f1 , real time polymerase chain reaction , gene expression , microbiology and biotechnology , biology , carcinogenesis , chemistry , cancer research , genetics
Sulfur dioxide (SO 2 ) 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 SO 2 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 (real‐time 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 SO 2 inhalation. These results lead to a conclusion that SO 2 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 SO 2 . 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. © 2009 Wiley Periodicals, Inc. Environ Toxicol 2010.