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

Abstract

To assess the effects of neonicotinoid insecticides on fish, juvenile Chinese rare minnows (Gobiocypris rarus) were exposed to 0.1, 0.5, or 2.0mg/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 2.0mg/L imidacloprid and 0.5mg/L nitenpyram and dinotefuran treatments (p<0.05). CAT activity was significantly increased with 0.1mg/L nitenpyram (p<0.05), whereas it was significantly decreased in the 0.1 and 2.0mg/L dinotefuran treatment groups (p<0.05). Moreover, MDA content was significantly decreased in all imidacloprid treatments and in the 0.5 and 2.0mg/L dinotefuran treatments (p<0.05); however, it was significantly increased in the 0.1mg/L nitenpyram treatment (p<0.05). GSH content was significantly increased at all treatments except for the 0.5mg/L dinotefuran treatment (p<0.05). The transcript expression results showed that gstm mRNA expression was significantly inhibited by 0.5 and 2.0mg/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 0.5mg/L nitenpyram treatment (p<0.05). The results of the DNA damage assay showed that tail moments were significantly increased by the 2.0mg/L imidacloprid treatment (p<0.01), while tail DNA was significantly increased by 0.5 and 2.0mg/L imidacloprid, 2.0mg/L nitenpyram and all dinotefuran treatments (p<0.01). Moreover, olive tail moments were significantly increased by the 0.5 and 2.0mg/L imidacloprid and 2.0mg/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.