4.7 Article

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

Journal

ENVIRONMENTAL POLLUTION
Volume 233, Issue -, Pages 862-871

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.envpol.2017.12.036

Keywords

Neonicotinoids; Genotoxicity; Immunotoxicity; Chinese rare minnows (Gobiocypris rams)

Funding

  1. National Natural Science Foundation of China [21677165]
  2. Major International Joint Research Project of the National Natural Science Foundation of China [51420105012]

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Adverse 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 cytokines IL-6, INF-alpha, TNF-alpha, and IL-1 beta were markedly down-regulated after all imidacloprid treatments (p<.05), whereas the expression levels of only TNF-alpha and IL-beta were 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. (C) 2017 Elsevier Ltd. All rights reserved.

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