Neonicotinoids caused oxidative stress and DNA damage in juvenile Chinese rare minnows (Gobiocypris rarus)

被引:34
作者
Tian, Xue [1 ,2 ,3 ]
Hong, Xiangsheng [3 ]
Yan, Saihong [3 ]
Li, Xiaoliang [2 ]
Wu, Huihui [1 ]
Lin, Aijun [1 ]
Yang, Wenjie [2 ,4 ]
机构
[1] Beijing Univ Chem Technol, Coll Chem Engn, 15 Beisanhuandonglu Rd, Beijing 100029, Peoples R China
[2] Chinese Acad Environm Planning, Beijing 100012, Peoples R China
[3] Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, Peoples R China
[4] North China Elect Power Univ, Coll Renewable Energy, Beijing 102206, Peoples R China
基金
中国国家自然科学基金;
关键词
Neonicotinoid insecticides; Oxidative stress; DNA damage; qRT-PCR; Chinese rare minnow (Gobiocypris rarus); ANTIOXIDANT ENZYME-SYSTEM; ATRAZINE EXPOSURE; IONIC LIQUID; ZEBRAFISH; INDUCTION; INSECTICIDES; ECOTOXICITY; DINOTEFURAN; EXPRESSION; BIOMARKERS;
D O I
10.1016/j.ecoenv.2020.110566
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
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.
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页数:8
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