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Title: Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats

Abstract

Sulfur dioxide (SO{sub 2},) 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 {+-} 3.44mg/m{sup 3} SO{sub 2} for 6h/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-polymerise 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 56.00mg/m{sup 3} SO{sub 2} the increases were significant (for p53: 1.23-fold at 28 mg/m{sup 3} and 1.39-fold at 56 mg/m{sup 3}; for bax: 1.77-fold at 28 mg/m{sup 3} and 2.26-fold at 56 mg/m{sup 3}, respectively), while mRNA levels of bcl-2 were decreased significantly (0.78-fold at 28 mg/m{sup 3} and 0.73-fold at 56 mg/m{sup 3}) in lungs of rats exposed to SO{sub 2}.more » Dose-dependent increase of p53 and bax proteins in the lungs was observed after SO{sub 2} inhalation, while decrease of bcl-2 protein levels was obtained using immunohistochemistry method. Caspase-3 activities were increased in lungs of rats after SO{sub 2} inhalation. These results lead to a conclusion that SO{sub 2}, exposure can change the expression of apoptosis-related genes, and it suggests that SO{sub 2} can induce apoptosis in lung of rat and may have relations with some apoptosis-related diseases. Elucidating the expression patterns of those factors after SO{sub 2} inhalation may be critical to our understanding mechanisms of SO{sub 2} toxicity and helpful for the therapeutic intervention.« less

Authors:
;  [1]
  1. Shanxi University, Taiyuan (China)
Publication Date:
OSTI Identifier:
20700879
Resource Type:
Journal Article
Resource Relation:
Journal Name: Regulatory Toxicology and Pharmacology; Journal Volume: 43; Journal Issue: 3
Country of Publication:
United States
Language:
English
Subject:
01 COAL, LIGNITE, AND PEAT; SULFUR DIOXIDE; RATS; AIR POLLUTION; LUNGS; INHALATION; HEALTH HAZARDS; GENES; EXPOSURE CHAMBERS; PROTEINS

Citation Formats

Bai, J.L., and Meng, Z.Q. Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats. United States: N. p., 2005. Web. doi:10.1016/j.yrtph.2005.09.002.
Bai, J.L., & Meng, Z.Q. Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats. United States. doi:10.1016/j.yrtph.2005.09.002.
Bai, J.L., and Meng, Z.Q. Thu . "Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats". United States. doi:10.1016/j.yrtph.2005.09.002.
@article{osti_20700879,
title = {Effects of sulfur dioxide on apoptosis-related gene expressions in lungs from rats},
author = {Bai, J.L. and Meng, Z.Q.},
abstractNote = {Sulfur dioxide (SO{sub 2},) 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 {+-} 3.44mg/m{sup 3} SO{sub 2} for 6h/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-polymerise 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 56.00mg/m{sup 3} SO{sub 2} the increases were significant (for p53: 1.23-fold at 28 mg/m{sup 3} and 1.39-fold at 56 mg/m{sup 3}; for bax: 1.77-fold at 28 mg/m{sup 3} and 2.26-fold at 56 mg/m{sup 3}, respectively), while mRNA levels of bcl-2 were decreased significantly (0.78-fold at 28 mg/m{sup 3} and 0.73-fold at 56 mg/m{sup 3}) in lungs of rats exposed to SO{sub 2}. Dose-dependent increase of p53 and bax proteins in the lungs was observed after SO{sub 2} inhalation, while decrease of bcl-2 protein levels was obtained using immunohistochemistry method. Caspase-3 activities were increased in lungs of rats after SO{sub 2} inhalation. These results lead to a conclusion that SO{sub 2}, exposure can change the expression of apoptosis-related genes, and it suggests that SO{sub 2} can induce apoptosis in lung of rat and may have relations with some apoptosis-related diseases. Elucidating the expression patterns of those factors after SO{sub 2} inhalation may be critical to our understanding mechanisms of SO{sub 2} toxicity and helpful for the therapeutic intervention.},
doi = {10.1016/j.yrtph.2005.09.002},
journal = {Regulatory Toxicology and Pharmacology},
number = 3,
volume = 43,
place = {United States},
year = {Thu Dec 01 00:00:00 EST 2005},
month = {Thu Dec 01 00:00:00 EST 2005}
}