苯并三唑和镉对斑马鱼肝脏的联合毒性效应

采用转基因斑马鱼Tg (lfabp10a: dsRed; elaA:EGFP)为模型,探讨了环境中苯并三唑及其衍生物(BTRs)与重金属镉对斑马鱼的单独与联合肝脏毒性效应.结果表明,0.001~0.1μmol/L CdCl2单独暴露使斑马鱼肝脏结合蛋白基因lfabp10a表达量增强,肝脏尺寸相对空白对照组显著膨大(P<0.005),而1μmol/L CdCl2显著抑制斑马鱼lfabp10a的表达,肝脏尺寸相对空白对照组显著降低(P<0.005).苯并三唑(1H-BTR,1H-benzotriazole)相对CdCl2而言毒性较低,5 μmol/L 1H-BTR暴露时斑马鱼肝脏lfabp10a表达量增强(P=0.000).联合暴露研究发现,1H-BTR能显著降低重金属镉对斑马鱼的肝脏毒性.因此, 苯并三唑在环境污染物毒性评价中具有重要意义.

Joint toxicity of benzotriazole and cadmium to zebrafish liver

Transgenic zebrafish Tg (lfabp10a: dsRed; elaA:EGFP) was used to explore the single and joint hepatotoxicities of benzotriazole and its derivatives (BTRs) and cadmium in the environment. The results showed that, the expression of liver-type fatty acid binding protein related gene lfabp10a in zebrafish was up-regulated under the exposure of 0.001 to 0.1μmol/L CdCl2, and the size of the liver was significant enlarged than that in the control group (P<0.005). But the expression of lfabp10a in zabrafish liver was inhibited by 1 μmol/L CdCl2, and the liver size was apparently decreased (P<0.005). Toxicity of 1H-BTR (1H-benzotriazole) was much lower when compared with that of CdCl2, and lfabp10a expressed in zebrafish liver was up-regulated under exposure of 5μmol/L 1H-BTR. The hepatotoxicity of CdCl2 was significantly reduced by 1H-BTR (P=0.000) in their combined exposure. Therefore, benzotriazole plays an important role in the evaluation of the toxicities of environmental pollutants.