Changes of hematological and biochemical parameters revealed genotoxicity and immunotoxicity of neonicotinoids on Chinese rare minnows (Gobiocypris rarus)

摘要

AbstractAdverse impacts of immunity in terrestrial non-target organisms exposed to neonicotinoid insecticides have been reported, but the causal link between insecticide exposure and possible immune alterations in fish remains limited. In the present study, the potential genotoxicity and immunotoxicity of three neonicotinoids (imidacloprid, nitenpyram, and dinotefuran) were assessed in Chinese rare minnows by using a 60-day chronic toxicity test. The hematological and biochemical parameters of juvenile Chinese rare minnows and changes in the transcription of six inflammation-related genes were determined after exposure to neonicotinoids at 0.1, 0.5, or 2.0 mg/L. A clear difference in the frequency of erythrocytes with micronuclei (MN) was observed after treatment with 2.0 mg/L imidacloprid (p < .05). Additionally, exposure to 0.5 or 2.0 mg/L imidacloprid significantly increased the binucleated (BN) erythrocytes and those with notched nuclei (NT) (p < .05). A serum protein electrophoresis (SPE) assay showed significant alterations in the serum protein in all treatments (p < .05), and further analysis indicated decreases in immunoglobulin (Ig) in treatments with 0.5 or 2.0 mg/L imidacloprid or dinotefuran or with 0.1 mg/L nitenpyram (p < .05). Moreover, a biochemical assay confirmed that immunoglobulin M (IgM) levels were indeed significantly decreased upon treatment with imidacloprid or dinotefuran at 0.5 or 2.0 mg/L (p < .05). In addition, the transcriptional levels of the inflammatory cytokinesIL-6,INF-α,TNF-α, andIL-1βwere markedly down-regulated after all imidacloprid treatments (p < .05), whereas the expression levels of onlyTNF-αandIL-1βwere significantly down-regulated following the 0.5 and 2.0 mg/L dinotefuran treatments (p < .05). Taken together, our results clearly demonstrate that imidacloprid, rather than nitenpyram and dinotefuran, can induce genotoxicity. The responsiveness of these immune indicators provides new insight into and evidence of the adverse effects of neonicotinoids on aquatic non-target organisms.Graphical abstractDisplay OmittedHighlights•Imidacloprid, but not nitenpyram and dinotefuran, can induce genotoxicity in aquatic fish.•The SPE assay indicated that chronic neonics exposure triggered an immune system related protein response in fish serum.•Transcript levels of inflammatory cytokines and chemokines are more sensitive to imidacloprid and dinotefuran.•Chronic imidacloprid and dinotefuran exposure might significantly decreases the immune system of juvenile fish.This study increases the understanding of the potential genotoxicity and immunotoxicity of neonicotinoids toward aquatic non-target organisms.