首页> 外文期刊>Toxicology Reports >Imidacloprid exposure cause the histopathological changes, activation of TNF-α, iNOS, 8-OHdG biomarkers, and alteration of caspase 3, iNOS, CYP1A, MT1 gene expression levels in common carp ( Cyprinus carpio L.)
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Imidacloprid exposure cause the histopathological changes, activation of TNF-α, iNOS, 8-OHdG biomarkers, and alteration of caspase 3, iNOS, CYP1A, MT1 gene expression levels in common carp ( Cyprinus carpio L.)

机译:吡虫啉暴露引起鲤的组织病理学改变,TNF-α,iNOS,8-OHdG生物标志物的活化以及胱天蛋白酶3,iNOS,CYP1A,MT1基因表达水平的改变。

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Imidacloprid (IMI) is a neonicotinoid that is widely used for the protection of crops and carnivores from insects and parasites, respectively. It is well known that imidacloprid exposure has a harmful effect on several organisms. However, there is little information about imidacloprid toxicity in aquatic animals, particularly fish. Thus, in the current study, we assessed the histopathological changes; activation of iNOS, 8-OHdG and TNF-α; and expression levels of caspase 3, iNOS, CYP1A and MT1 genes in the common carp exposed to imidacloprid. For this purpose, fish were exposed to either a low dose (140?mg/L) or a high dose (280?mg/L) of imidacloprid for 24?h, 48?h, 72?h and 96?h. After IMI exposure, we detected hyperplasia of secondary lamellar cells and mucous cell hyperplasia in the gills, as well as hydropic degeneration in hepatocytes and necrosis in the liver. Moreover, 8-OHdG, iNOS and TNF-α activation was found particularly in the gills and liver but also moderately in the brain. Transcriptional analysis showed that caspase 3 expression was altered low dose and high doses of IMI for 72?h and 96?h exposure ( p? ?0.05), iNOS expression was up-regulated with both low and high doses of IMI and in a time-dependent manner ( p?? 0.05, p? ?0.01, p?? 0.001), CYP1A expression was not significantly changed regardless of the dose of IMI and exposure time ( p?? 0.05) except with low and high doses of IMI for 96?h ( p? ?0.05), and lastly, MT1 gene expression was up-regulated only in the brain with low doses of IMI for 96?h and high doses of IMI for 48?h, 72?h and 96?h exposure ( p? ?0.05, p? ?0.01). Our results indicated that acute IMI exposure moderately induce apoptosis in the brain but caused severe histopathological lesions, inflammation, and oxidative stress in the gills, liver, and brain of the common carp.
机译:吡虫啉(IMI)是一种新烟碱,广泛用于保护农作物和食肉动物免受昆虫和寄生虫侵害。众所周知,吡虫啉暴露对几种生物都有有害作用。但是,关于吡虫啉对水生动物特别是鱼类的毒性的信息很少。因此,在本研究中,我们评估了组织病理学变化。 iNOS,8-OHdG和TNF-α的激活;吡虫啉对鲤的半胱氨酸天冬氨酸蛋白酶3,iNOS,CYP1A和MT1基因表达水平的影响为此目的,将鱼暴露于低剂量(140?mg / L)或高剂量(280?mg / L)吡虫啉24小时,48小时,72小时和96小时。 IMI暴露后,我们检测到secondary中继发性片状细胞增生和粘液细胞增生,以及肝细胞的水样变性和肝脏坏死。此外,特别是在the和肝脏中发现了8-OHdG,iNOS和TNF-α的激活,但在大脑中也发现了中等程度的激活。转录分析显示,低剂量和高剂量的IMI在暴露72?h和96?h时caspase 3的表达发生了改变(p 0.05),iNOS的表达在高,低剂量的IMI中均被上调。时间依赖性(p <0.05,p <0.01,p <0.001),CYP1A的表达与IMI剂量和暴露时间无关(p <0.05),而低和低高剂量IMI持续96?h(p 0.05),最后,MT1基因表达仅在低剂量IMI持续96?h而高剂量IMI持续48?h的大脑中被上调,72 Δh和96°h暴露(p <0.05,p <0.01)。我们的结果表明,急性IMI暴露可适度诱导脑细胞凋亡,但会引起鲤的,肝和脑严重组织病理学损伤,炎症和氧化应激。

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