Nanopolystyrene and phoxim pollution: A threat to hepatopancreas toxicity in Chinese mitten crab (Eriocheir sinensis)

•NP and/or PHO exposure causes hepatopancreatic inflammation.•NP and/or PHO exposure induces hepatopancreas oxidative stress in Eriocheir sinensis.•Combined exposure may exacerbate hepatopancreas injury. Significant concerns have been raised by the widespread pollutants phoxim (PHO) and nanopolystyr...

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Veröffentlicht in:Aquatic toxicology 2024-11, Vol.276, p.107124, Article 107124
Hauptverfasser: Huang, Mengting, Ma, Yuan, Che, Shunli, Shen, Longteng, Wan, Zhicheng, Su, Shiping, Ding, Shuquan, Li, Xilei
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Sprache:eng
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Zusammenfassung:•NP and/or PHO exposure causes hepatopancreatic inflammation.•NP and/or PHO exposure induces hepatopancreas oxidative stress in Eriocheir sinensis.•Combined exposure may exacerbate hepatopancreas injury. Significant concerns have been raised by the widespread pollutants phoxim (PHO) and nanopolystyrene (NP) in the natural environment. This study evaluated the toxicity effects on the hepatopancreas of Eriocheir sinensis caused by NP and/or PHO at concentrations found in the environment. Subchronic exposure to NP and/or PHO triggered hepatopancreas histological damage within a 21-day exposure period. The NP, PHO, and co-exposure (NPO) groups exhibited fewer blister-like (B) cells, along with the appearance of vacuolation. Furthermore, these exposures induced impairment in the hepatic tubule mucus barrier and mechanical barrier, as evidenced by altered expression of oxidative stress-related genes, mucin-related genes, and TJ-related genes. Additionally, alterations in immunity-related genes and inflammatory cytokine genes expression were observed. The findings showed that hepatopancreas inflammation was caused by both individual and combined exposure to NP and PHO and that the inflammatory response was exacerbated by the co-exposure. The possible pathways of hepatopancreas toxicity were further investigated by transcriptomic analysis. Hepatopancreas inflammation was brought on by subchronic exposure to PHO and co-exposure; this inflammation was exacerbated by co-exposure and was backed by the activation of NF-κB signaling pathway via targeting-related genes. In summary, this research represents the initial documentation, to the best of our understanding of the detrimental effects of exposured to NP and/or PHO at levels found in the environment disrupt the hepatopancreas mucus and mechanical barrier in crustaceans, triggering inflammatory responses. These findings highlight the significance of NP and/or PHO pollution for hepatopancreas health. [Display omitted]
ISSN:0166-445X
1879-1514
1879-1514
DOI:10.1016/j.aquatox.2024.107124