College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.
Henan International Joint Laboratory of Aquatic Toxicology and Health Protection, Henan Normal University, Xinxiang, Henan 453007, China.
Pestic Biochem Physiol. 2024 Feb;199:105799. doi: 10.1016/j.pestbp.2024.105799. Epub 2024 Jan 25.
Fenpropathrin (FEN), a pyrethroid pesticide, is frequently detected in natural water bodies, unavoidable pose adverse effects to aquatic organisms. However, the harmful effects and potential mechanisms of FEN on aquatic species are poorly understood. In this study, common carp were treatment with FEN at 0.45 and 1.35 μg/L for 14 d, and the toxic effects and underlying mechanisms of FEN on the intestine of carp were revealed. RNA-seq results showed that FEN exposure cause a wide range of transcriptional alterations in the intestine and the differentially expressed genes were mainly enrichment in the pathways related to immune and metabolism. Specifically, FEN exposure induced pathological damage and altered submicroscopic structure of the intestine, elevated the levels of Bacteroides fragilis enterotoxin, altered the contents of claudin-1, occludin, and zonula occluden-1 (ZO-1), and causing injury to the intestinal barrier. In addition, inflammation-related index TNF-α in the serum and IL-6 in the intestinal tissues were generally increased after FEN exposure. Moreover, FEN exposure promoted an increase in reactive oxygen species (ROS), altered the levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), upregulated the contents of malondialdehyde (MDA) in the intestines. The apoptosis-related parameter cytochrome c, caspase-9, and caspase-3 were significantly altered, indicating that inflammation reaction, oxidative stress, and apoptosis may be involved in the toxic mechanism of FEN on carp. Moreover, FEN treatment also altered the intestinal flora community significantly, which may affect the intestinal normal physiological function and thus affect the growth of fish. Overall, the present study help to clarify the intestinal reaction mechanisms after FEN treatment, and provide a basis for the risk assessment of FEN.
氯菊酯(FEN)是一种拟除虫菊酯类农药,经常在天然水体中被检测到,不可避免地对水生生物产生不利影响。然而,FEN 对水生物种的有害影响和潜在机制尚不清楚。在这项研究中,用 0.45 和 1.35μg/L 的 FEN 处理鲤鱼 14 天,揭示了 FEN 对鲤鱼肠道的毒性作用和潜在机制。RNA-seq 结果表明,FEN 暴露会导致肠道广泛的转录变化,差异表达基因主要富集在与免疫和代谢相关的途径中。具体来说,FEN 暴露会引起肠道的病理损伤和超微结构改变,增加脆弱拟杆菌肠毒素的水平,改变紧密连接蛋白-1、闭合蛋白和闭合小带蛋白-1(ZO-1)的含量,导致肠道屏障损伤。此外,FEN 暴露后血清中炎症相关指标 TNF-α和肠道组织中 IL-6 普遍升高。此外,FEN 暴露会促进活性氧(ROS)的增加,改变超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽(GSH)的水平,增加肠道丙二醛(MDA)的含量。细胞色素 c、caspase-9 和 caspase-3 等凋亡相关参数明显改变,表明炎症反应、氧化应激和细胞凋亡可能参与了 FEN 对鲤鱼的毒性机制。此外,FEN 处理还显著改变了肠道菌群群落,这可能会影响肠道的正常生理功能,从而影响鱼类的生长。总之,本研究有助于阐明 FEN 处理后肠道的反应机制,为 FEN 的风险评估提供依据。