4.7 Article

Acute thiamethoxam exposure induces hepatotoxicity and neurotoxicity in juvenile Chinese mitten crab (Eriocheir sinensis)

Journal

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 249, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2022.114399

Keywords

Neonicotinoid pesticides; Crustacean; Oxidative stress; Detoxification; Synaptic transmission; Toxicity

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The study found that thiamethoxam, a neonicotinoid insecticide, can be toxic to crustaceans, leading to hepatotoxicity and neurotoxic effects. The toxicity is related to the activation of antioxidant and detoxification systems, regulation of immune-related gene expression, and potential inflammatory response. High concentrations of thiamethoxam also cause decreased acetylcholinesterase activity and downregulation of synaptic transmission-related genes, affecting neurotoxicity in crustaceans.
The similar nervous system structure between crustaceans and insects and the high-water solubility of thiame-thoxam can lead to the more severe toxicity of thiamethoxam to crustaceans. However, the effects of thiame-thoxam on crustaceans are unclear. Therefore, a 96-h acute toxicity test was performed to explore the hepatotoxicity and neurotoxicity effects of thiamethoxam on Chinese mitten crab (Eriocheir sinensis) at con-centrations 0 mu g/L, 150 mu g/L and 300 mu g/L. The antioxidant and detoxification systems (including phases I and II) were significantly activated after exposure of juvenile crabs to thiamethoxam for 24 h in 300 mu g/L group, whereas the toxic activation effect in 150 mu g/L group was delayed. Moreover, a similar pattern was observed for the transcription levels of immune-related genes. Further analysis of inflammatory signaling pathway-related genes showed that thiamethoxam exposure with 300 mu g/L for 24 h may induce a pro-inflammatory response through the NF-kappa B pathway. In contrast, the gene expression levels in 150 mu g/L group were significantly upre-gulated compared with 0 mu g/L group after 96 h. In addition, although the acute exposure of 150 mu g/L thiame-thoxam did not seem to induce significant neurotoxicity, the acetylcholinesterase activity was significantly decreased in 300 mu g/L group after thiamethoxam exposure for 96 h. Correspondingly, thiamethoxam exposure with 300 mu g/L for 24 h resulted in significantly downregulated transcriptional levels of synaptic transmission -related genes (e.g. dopamine-, gamma-aminobutyric acid-and serotonin-related receptors). Therefore, thiame-thoxam may be harmful and cause potential toxic threats such as neurotoxicity and metabolic damage to crustaceans.

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