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Joint toxicity of benzotriazole and cadmium to zebrafish liver |
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Abstract 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.
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Received: 10 November 2014
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