Kitajima H, Hirano S, Suzuki K T
Faculty of Pharmaceutical Sciences, Chiba University, 1-33 Yayoi, Inage Chiba 263-8522, Japan.
Arch Toxicol. 1999 Sep;73(7):410-2. doi: 10.1007/s002040050681.
Inhalation exposure to cadmium (Cd) is associated with inflammatory lesion in the lung. In the present study we have investigated cytotoxic effects of Cd on immortalized rat lung epithelial cells (SV40-T2) and gene expression in those cells following in vitro exposure to sublethal concentrations of cadmium chloride (CdCl(2)). The polymerase chain reaction (PCR)-based subtraction method was used to find differentially expressed genes between control and Cd-exposed SV40-T2 cells. The most prominent cDNA on an agarose gel was identical to a fragment of rat heme oxygenase (HO) gene. Northern blot analysis indicated that the level of HO mRNA expression in SV40-T2 cells was increased to 38-fold of the control value following exposure to 2.5 microM CdCl(2) for 4 h. These results suggest that HO gene expression is one of the most sensitive biomarkers for acute exposure to Cd in the lung.
吸入镉（Cd）与肺部炎症性病变有关。在本研究中，我们调查了镉对永生化大鼠肺上皮细胞（SV40-T2）的细胞毒性作用，以及在体外暴露于亚致死浓度的氯化镉（CdCl₂）后这些细胞中的基因表达情况。采用基于聚合酶链反应（PCR）的消减方法来寻找对照和镉暴露的SV40-T2细胞之间差异表达的基因。琼脂糖凝胶上最明显的cDNA与大鼠血红素加氧酶（HO）基因的一个片段相同。Northern印迹分析表明，在暴露于2.5微摩尔/升CdCl₂ 4小时后，SV40-T2细胞中HO mRNA的表达水平增加到对照值的38倍。这些结果表明，HO基因表达是肺部急性镉暴露最敏感的生物标志物之一。
