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Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats.
Regul Toxicol Pharmacol. 2005 Dec; 43(3):272-9.RT

Abstract

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.

Authors+Show Affiliations

Institute of Environmental Medicine and Toxicology, Shanxi University, Taiyuan 030006, China. baijuli@sxu.edu.cnNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16256253

Citation

Bai, Juli, and Ziqiang Meng. "Effects of Sulfur Dioxide On Apoptosis-related Gene Expressions in Lungs From Rats." Regulatory Toxicology and Pharmacology : RTP, vol. 43, no. 3, 2005, pp. 272-9.
Bai J, Meng Z. Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats. Regul Toxicol Pharmacol. 2005;43(3):272-9.
Bai, J., & Meng, Z. (2005). Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats. Regulatory Toxicology and Pharmacology : RTP, 43(3), 272-9.
Bai J, Meng Z. Effects of Sulfur Dioxide On Apoptosis-related Gene Expressions in Lungs From Rats. Regul Toxicol Pharmacol. 2005;43(3):272-9. PubMed PMID: 16256253.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats. AU - Bai,Juli, AU - Meng,Ziqiang, Y1 - 2005/10/26/ PY - 2005/07/31/received PY - 2005/11/1/pubmed PY - 2006/2/1/medline PY - 2005/11/1/entrez SP - 272 EP - 9 JF - Regulatory toxicology and pharmacology : RTP JO - Regul Toxicol Pharmacol VL - 43 IS - 3 N2 - 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. SN - 0273-2300 UR - https://www.unboundmedicine.com/medline/citation/16256253/Effects_of_sulfur_dioxide_on_apoptosis_related_gene_expressions_in_lungs_from_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0273-2300(05)00169-8 DB - PRIME DP - Unbound Medicine ER -