The effects of fipronil exposure on oxidative stress, non-specific immunity, autophagy, and apoptosis in the common carp.

The increase in the area treated with the insecticide fipronil has caused concern for aquatic organisms such as fish. Here, we assessed the effect of fipronil on carp indexes of non-specific immunity, oxidative stress, autophagy, and apoptosis following exposure to 0.074 mg/L and 0.185 mg/L of fipronil in the aqueous environment for 1 day, 3 days, 5 days, and 7 days. It was found that glutathione (GSH), malonaldehyde (MDA), and superoxide dismutase (SOD) in gills were significantly reduced (P < 0.05). The increase in exposure time increases the impact on GSH, SOD, and MDA parameters in the liver and intestine. Liver acid phosphatase (ACP), alkaline phosphatase (AKP), and lysozyme (LZM) activity levels increased significantly in the treatment group on the first day after exposure, except for the 0.074 mg/L group of ACP (P < 0.05). The mRNA expression levels of autophagy-related genes ATG12, ATG5, ATG16L, LC3-II, and BECN1 were generally elevated in the liver and intestine during the initial exposure period (P < 0.05), while mTOR was significantly reduced on the first and third days after treatment (P < 0.05). From the results of Western blotting (WB), we can see that the amount of LC3-II was significantly higher than that of LC3-I at 1, 3, and 5 days of exposure (P < 0.05). Furthermore, the apoptosis-related gene Bcl-2 reached its peak in the liver, intestine, and gill on the first day, and caspase3 was significantly downregulated throughout the exposure period (P < 0.05). The results showed that fipronil was potentially harmful to carp and should be used moderately to reduce the damage to aquatic ecosystems. This study complements the mechanism theory of fipronil on fish toxicology and has a certain value for human health risk assessment.