摘要:
为研究新型阻燃剂磷酸三(2,3-二氯丙基)酯(TDCPP)的毒性效应,以稀有鮈鲫(Gobiocypris rarus)为实验生物,采用半静态实验方法,分别进行96 h和28 d的染毒,研究TDCPP对稀有鮈鲫的急性毒性和慢性毒性效应,并通过对稀有鮈鲫脑组织中与神经纤维的生长、发育、轴突再生等相关基因mRNA表达量的检测,初步探讨了TDCPP的神经毒性作用。结果表明:TDCPP对稀有鮈鲫的96 h-LC50为2.99(2.20~3.38) mg·L-1,根据化学物质对鱼类毒性分级标准TDCPP属于剧毒性。经0.9、1.5、2.1和2.7 mg·L-1 TDCPP染毒28 d,与对照组相比,暴露组稀有鮈鲫肝脏及脑组织中SOD和GSH-Px的活性均受到抑制,且随着TDCPP的暴露浓度增加,其抑制作用显著增强;暴露组稀有鮈鲫脑组织中与神经纤维的生长、发育相关的微管蛋白α/β、神经丝NF-M以及关键蛋白GAP-43等基因的mRNA表达量,与对照相比均发生显著下调。可知,TDCPP暴露可以诱发稀有鮈鲫神经毒性作用。
Abstract:
Toxicological effects of tri(2,3-dichloroprophyl) phosphate (TDCPP) on rare minnow (Gobiocypris rarus) were investigated using the semi-static bioassay, including 96 h acute toxicity and 28 d chronic toxicity. We also explored some special gene expression levels such as NF-M, GAP-43, Tubulin α/β, which resulted in neurotoxicity of TDCPP. Results showed that the 96 h-LC50 value of TDCPP to rare minnow was 2.99 (2.20~3.38) mg·L-1. According to the criteria for evaluating and grading toxicity of chemicals to fishes, the toxicity of TDCPP should be the hypertoxicity level. The activities of SOD and GSH-Px in both liver and brain tissues of rare minnow were inhibited in comparison with the control, after exposure to 0.9, 1.5, 2.1 and 2.7 mg·L-1 TDCPP for 28 d. The inhibition strengthened as TDCPP concentration increased. Furthermore, the expressions of specific genes in brain tissue involved in neurotrophic factor, such as NF-M, GAP-43 and microtubulin α/β were significantly down-regulated compared with the control. It is indicated that TDCPP may induce the neurotoxic effect on rare minnow.