Data for: DNA damage in liver cells of the tilapia fish Oreochromis mossambicus larva induced by the insecticide cyantraniliprole at sublethal doses during chronic exposure

This paper described the acute and chronic toxicity of cyantraniliprole to juvenile tilapia was evaluated in the present study. The results showed that 96 h LC50 of cyantraniliprole to tilapia was 38 mg/L. After exposure for 28 days, specific growth rates of the blank control, solution control, and the treatments of 0.037, 0.37 and 3.7 mg/L of cyantraniliprole were 1.14, 0.95, 0.93, 0.82 and 0.70% per day, respectively. The results of micronucleus experiment and single cell gel electrophoresis showed that cyantraniliprole damaged DNA in liver cells of tilapia larvae. Quantitative PCR results showed that cyantraniliprole could induce the up-regulation of the genes Ccne 1, Cdk2, Orc1, Ccna 1, Ccnb, Rpa 3 and Fen1 that are responsible for the DNA damage and repair. Among those genes, Ccna1 and Rpa3 were most notably up-regulated. It is therefore proposed that cyantraniliprole causes DNA damage in liver cells of tilapia and activates DNA damage and repair pathways.

本研究评估了氰氟虫腙（cyantraniliprole）对幼罗非鱼的急性与慢性毒性，相关内容已在本文中阐述。研究结果显示，氰氟虫腙对罗非鱼的96小时半数致死浓度（LC50）为38 mg/L。经28天暴露后，空白对照组、溶剂对照组以及0.037、0.37、3.7 mg/L氰氟虫腙处理组的特定生长率分别为每日1.14%、0.95%、0.93%、0.82%和0.70%。微核试验与单细胞凝胶电泳结果表明，氰氟虫腙可损伤罗非鱼幼鱼肝细胞的DNA。定量PCR（Quantitative PCR）结果显示，氰氟虫腙可诱导参与DNA损伤与修复的Ccne1、Cdk2、Orc1、Ccna1、Ccnb、Rpa3及Fen1基因表达上调。其中，Ccna1与Rpa3的表达上调最为显著。综上，本研究表明氰氟虫腙可造成罗非鱼肝细胞DNA损伤，并激活DNA损伤与修复通路。