Details

Autor(en) / Beteiligte

• Wang, Wenhua
• Mou, Shaoyu
• Xiu, Wenyao
• Li, Yuanyuan
• Liu, Zhihui
• Feng, Yiyi
• Ma, Junguo
• Li, Xiaoyu

Titel

Fenpropathrin disrupted the gills of common carp (Cyprinus carpio L.) through oxidative stress, inflammatory responses, apoptosis, and transcriptional alterations

Ist Teil von

• Ecotoxicology and environmental safety, 2024-02, Vol.271, p.116007-116007, Article 116007

Ort / Verlag

Netherlands: Elsevier Inc

Erscheinungsjahr

2024

Quelle

MEDLINE

Beschreibungen/Notizen

• Fenpropathrin (FEN) is an extensively utilized synthetic pyrethroid insecticide frequently found in aquatic ecosystems. However, the adverse effects and potential mechanisms of FEN on aquatic species are poorly understood. In this work, common carp were treated with FEN at concentrations of 0.45 and 1.35 μg/L FEN for 14 days, after which the tissue structure, physiological alterations, and mRNA transcriptome of the gills were evaluated. Specifically, FEN exposure caused pathological damage to the gills of carp, downregulated the levels of claudin-1, occludin, and zonula occluden-1 (ZO-1), and inhibited Na+-K+-ATPase activity in the gills. In addition, FEN exposure promoted an increase in reactive oxygen species (ROS) levels and significantly upregulated the levels of malondialdehyde (MDA), 8-hydroxy-2 deoxyguanosine (8-OHdG), and protein carbonyl (PC) in the gills. Moreover, the inflammation-related indices (TNF-α, IL-1β, and IFN-γ) and the apoptosis-related parameter caspase-3 were generally increased, especially in the 1.35 μg/L FEN group, and these indices were significantly greater than those in the control group. These findings suggest that FEN exposure can cause oxidative stress, the inflammatory response, and apoptosis in carp gills. Importantly, the results of RNA-seq analysis showed that 0.45 and 1.35 μg/L FEN could significantly interfere with multiple immune and metabolic pathways, including the phagosome, NOD-like receptor (NLR) signalling pathway, Toll-like receptor (TLR) signalling pathway, necroptosis, and arachidonic acid metabolism pathways, indicating that the effects of FEN on the gills of fish are intricate. In summary, our findings confirm the toxic effects of FEN on common carp gills and provide additional comprehensive information for evaluating the toxicity and underlying molecular mechanisms of FEN in aquatic organisms. [Display omitted] •FEN exposure altered the Na+-K+-ATPase activities and TJ proteins levels in the carp gills.•Oxidative stress, inflammatory response, and apoptosis were observed under FEN stress.•FEN treatment induced transcriptional alterations in carp gills.•TLR and NLR signaling pathways may participate in FEN caused gill toxicity.•FEN exposure disturbed structure and function of gills in common carp.