Expression of apoptosis-related genes in livers from rats exposed to sulfur dioxide
Expression of apoptosis-related genes in livers from rats exposed to sulfur dioxide
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DOI：
10.1016/j.tox.2005.08.016
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发表时间：
2005-12-15
期刊：
影响因子：
4.5
通讯作者：
Meng, ZQ
中科院分区：
文献类型：
--
作者：
Bai, JL;Meng, ZQ
二氧化硫（SO2）是一种普遍存在的空气污染物，在城市空气中浓度较低，在工作环境中浓度较高。本研究将雄性Wistar大鼠置于暴露室中，分别以14.00 +/- 1.01、28.00 +/- 1.77和56.00 +/- 3.44 mg/m(3) SO2处理6h/d，连续7 d，对照组在相同条件下暴露于过滤空气中。采用实时逆转录聚合酶链式反应（real-time RT-PCR）和免疫组织化学方法分析肝脏中3个凋亡相关基因（p53和bax是凋亡启动子，bcl-2是凋亡抑制因子）的mRNA和蛋白水平。结果表明，在SO2浓度为28.00和56.00 mg/m(3)时，p53和bax的mRNA水平呈剂量依赖性增加(p53在28 mg/m(3)时为1.30倍，56 mg/m(3)时为3.43倍，bax在28 mg/m（3)时为1.63倍，56 mg/m(3)时为2.17倍），而bcl-2的mRNA水平则显著降低(28 mg/m（3)时为0.63倍，56 mg/m(3)时为0.45倍）。吸入SO2后肝脏中p53和bax蛋白呈剂量依赖性升高，免疫组化法观察bcl-2蛋白水平降低。这些结果表明，SO2暴露可改变凋亡相关基因的表达，提示SO2可诱导大鼠肝脏细胞凋亡，并可能与某些凋亡相关疾病有关。阐明吸入SO2后细胞凋亡信号通路相关因子的表达规律，对我们理解SO2毒性作用机制和治疗干预具有重要意义。2005爱思唯尔爱尔兰有限公司版权所有。
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 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 were promoters of apoptosis, whereas bcl-2 was apoptotic suppressor) were analyzed in livers using a real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay and immunohistochemistry method. 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/m(3) SO2 the increases were significant (for p53: 1.30-fold at 28 mg/m(3) and 3.43-fold at 56 mg/m(3), for bax: 1.63-fold at 28 mg/m(3) and 2.17-fold at 56 mg/m(3), respectively), while mRNA levels of bcl-2 were decreased significantly (0.63-fold at 28 mg/m(3) and 0.45-fold at 56 mg/m(3)) in livers of rats exposed to SO2. Dose-dependent increases of p53 and bax proteins in the livers were observed after SO2 inhalation, while decrease of bcl-2 protein levels was obtained using immunohistochemistry method. These results lead to a conclusion that SO2 exposure could change the expression of apoptosis-related genes, and it suggests that SO2 can induce apoptosis in liver of rat and may have relations with some apoptosis-related diseases. It is critical for our understanding of the mechanisms of SO2 toxicity and helpful for the therapeutic intervention to elucidate the expression pattern of those factors involved in apoptosis signaling pathway after SO2 inhalation. (c) 2005 Elsevier Ireland Ltd. All rights reserved.