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环境毒理

Upregulation of inhaled formaldehyde on the transcription of GSNO reductase gene in mice lungs

摘要：为了验证吸入甲醛及气道氧化还原状态变化可在转录水平调控GSNOR表达,研究了甲醛环境暴露和抗氧化剂α-硫辛酸对小鼠肺中GSNOR表达的影响.以昆明系小鼠为实验材料,经吸入甲醛染毒和α-硫辛酸注射后立即脱颈处死,取其肺组织提取总RNA,采用RT-PCR二步法将其中GSNOR及管家基因β-actin扩增后,通过光密度分析染毒前后基因转录水平的变化.实验结果表明,与对照组相比,3.0mg·m^-3浓度的甲醛可使GSNOR基因转录发生显著上调(p<0.01),而α-硫辛酸的注射可拮抗这种上调作用,表明吸入甲醛可在转录水平诱导GSNOR表达上调,而且这种上调与肺部的氧化还原状态改变有关,这可能是GSNOR在气道表达及其在哮喘发生中的作用基础.

Abstract：In order to test the hypothesis that formaldehyde and redox state in the airway could regulate GSNOR expression at the transcription level, effects of environmental formaldehyde exposure and antioxidant α-lipoic acid injection on GSNOR expression in mice lungs were investigated in the present study. Kunming purebred mice were used as experimental animals and the total RNAwas extracted from the lungs immediately after exposure to formaldehyde and injection with α-lipoic acid. RT-PCRwas applied to examine the transcriptional changes of GSNOR and β-actin which was used as the control gene. The results showed that compared with control groups, 3.0 mg·m^-3 formaldehyde exposure resulted in a significant increase of GSNOR expression ( p<0.01), and α-lipoic acid injection completely blocked the increase. These results suggest that inhaled gaseous formaldehyde could induce up-regulation of GSNOR at the transcription level, and the changes may be related to an altered redox state in the lungs, which might provide a basis for the understanding of GSNORexpression in lungs.