College of Chemical Engineering, Beijing University of Chemical Technology, Beijing, 100029, China; Chinese Academy for Environmental Planning, Beijing, 100012, China; Key Laboratory of Drinking Water Science and Technology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, 100085, China.
Key Laboratory of Drinking Water Science and Technology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, 100085, China.
Ecotoxicol Environ Saf. 2020 Jul 1;197:110566. doi: 10.1016/j.ecoenv.2020.110566. Epub 2020 Apr 10.
To assess the effects of neonicotinoid insecticides on fish, juvenile Chinese rare minnows (Gobiocypris rarus) were exposed to 0.1, 0.5, or 2.0 mg/L neonicotinoid insecticides (imidacloprid, nitenpyram, and dinotefuran) for 60 days. The endpoints, including oxidative stress and DNA damage, were determined. The results of oxidative stress assays showed that SOD activities were significantly increased in the 2.0 mg/L imidacloprid and 0.5 mg/L nitenpyram and dinotefuran treatments (p < 0.05). CAT activity was significantly increased with 0.1 mg/L nitenpyram (p < 0.05), whereas it was significantly decreased in the 0.1 and 2.0 mg/L dinotefuran treatment groups (p < 0.05). Moreover, MDA content was significantly decreased in all imidacloprid treatments and in the 0.5 and 2.0 mg/L dinotefuran treatments (p < 0.05); however, it was significantly increased in the 0.1 mg/L nitenpyram treatment (p < 0.05). GSH content was significantly increased at all treatments except for the 0.5 mg/L dinotefuran treatment (p < 0.05). The transcript expression results showed that gstm mRNA expression was significantly inhibited by 0.5 and 2.0 mg/L imidacloprid, and gstp1 mRNA expression was significantly inhibited by all nitenpyram treatments (p < 0.05). In addition, ugt1a mRNA expression was significantly inhibited in the 0.5 mg/L nitenpyram treatment (p < 0.05). The results of the DNA damage assay showed that tail moments were significantly increased by the 2.0 mg/L imidacloprid treatment (p < 0.01), while tail DNA was significantly increased by 0.5 and 2.0 mg/L imidacloprid, 2.0 mg/L nitenpyram and all dinotefuran treatments (p < 0.01). Moreover, olive tail moments were significantly increased by the 0.5 and 2.0 mg/L imidacloprid and 2.0 mg/L dinotefuran treatments (p < 0.01). Therefore, our oxidative stress and DNA damage findings demonstrated that imidacloprid and nitenpyram could cause adverse effects on juvenile rare minnows.
为了评估新烟碱类杀虫剂对鱼类的影响，将幼年稀有鲫（Gobiocypris rarus）暴露于 0.1、0.5 或 2.0mg/L 的新烟碱类杀虫剂（吡虫啉、吡虫清和噻虫嗪）中 60 天。测定了氧化应激和 DNA 损伤等终点指标。氧化应激测定结果表明，2.0mg/L 吡虫啉和 0.5mg/L 吡虫清和噻虫嗪处理组 SOD 活性显著升高（p<0.05）。CAT 活性在 0.1mg/L 吡虫清处理组显著升高（p<0.05），而在 0.1 和 2.0mg/L 噻虫嗪处理组显著降低（p<0.05）。此外，丙二醛含量在所有吡虫啉处理组和 0.5 和 2.0mg/L 噻虫嗪处理组均显著降低（p<0.05）；然而，在 0.1mg/L 吡虫清处理组显著增加（p<0.05）。GSH 含量除 0.5mg/L 噻虫嗪处理组外均显著升高（p<0.05）。转录表达结果表明，0.5 和 2.0mg/L 吡虫啉显著抑制 gstm mRNA 表达，所有吡虫清处理组均显著抑制 gstp1 mRNA 表达（p<0.05）。此外，0.5mg/L 吡虫清处理组 ugt1a mRNA 表达显著抑制（p<0.05）。DNA 损伤测定结果表明，2.0mg/L 吡虫啉处理组尾矩显著增加（p<0.01），而 0.5 和 2.0mg/L 吡虫啉、2.0mg/L 吡虫清和所有噻虫嗪处理组尾 DNA 显著增加（p<0.01）。此外，0.5 和 2.0mg/L 吡虫啉和 2.0mg/L 噻虫嗪处理组橄榄尾矩显著增加（p<0.01）。因此，我们的氧化应激和 DNA 损伤研究结果表明，吡虫啉和吡虫清可能对幼年稀有鲫产生不良影响。
