溴氰菊酯对凡纳滨对虾酶活性、细胞凋亡和免疫反应以及组织学形态的毒理学影响

IF 5.4 Q2 ENGINEERING, ENVIRONMENTAL
Kangyuan Qu , Sukma Melati , Junwei Zeng , Jiayu Li , Menglin Shi , Liutong Chen , Yucheng Liu , Shiwei Xie
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引用次数: 0

摘要

在农业生产和储存过程中使用溴氰菊酯(DM)会导致多种饲料成分中出现残留物,水生动物摄入这些残留物后可能会对健康产生不利影响。虽然已有多项研究对亲脂性溴氰菊酯的潜在毒性进行了评估,但关于对虾长期暴露于不同膳食脂质水平的溴氰菊酯所引起的负面影响的综合研究还很少。我们进行了一项为期六周的喂养实验,以评估膳食脂质水平的改变是否会对溴氰菊酯的毒性产生影响。在凡纳滨对虾的饲养实验中,研究了日粮脂肪水平对DM毒性的影响。实验中使用了六种不同的日粮,包括三种DM水平(0.2 mg-kg-1、1 mg-kg-1、5 mg-kg-1)和两种脂肪水平(6.96 %、10.88 %)。日粮分别为 LF0.2、LF1、LF5、HF0.2、HF1、HF5。结果表明,随着日粮中DM添加量的增加,对虾的生长性能和全身脂质均有所下降,并且在饲喂高剂量DM的日粮时,DM会导致对虾脂蛋白(低密度脂蛋白、高密度脂蛋白、低脂蛋白)发生异常变化。此外,研究还发现,长期接触DM会显著增加GOT、GPT、AKP和ACP的活性。同时,与核因子卡巴-B免疫信号通路相关的基因在对虾的肝胰腺(背侧、imd、颗粒、ikkβ)、肠道(imd、管状、颗粒)和肌肉(收费、imd、颗粒)中的表达方式在接触DM后出现了明显增加。同样,对虾长期暴露于 DM 后,肝胰腺(atg9、atg12)、肌肉(atg3、atg9)和肠道(atg3、atg5、atg9、beclin、atg13)中的细胞自噬基因以剂量依赖的方式显著上调。在DM暴露条件下,肌肉也会出现组织病理学损伤。总之,长期暴露于DM会导致生长性能减慢,脂蛋白代谢紊乱,肝胰腺、肠道和肌肉相关免疫功能受损,以及自噬的促进和对虾肌肉的损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Toxicological effect of deltamethrin on enzymatical, apoptosis and immune response, histological morphology in Litopenaeus vannamei

Toxicological effect of deltamethrin on enzymatical, apoptosis and immune response, histological morphology in Litopenaeus vannamei

Deltamethrin (DM) use in agricultural production and storage can result in the presence of residues in several feed ingredients, which can then be ingested by aquatic animals, potentially leading to adverse health effects. Although the potential toxicity of the lipophilic deltamethrin has been evaluated in several studies, there is a paucity of comprehensive studies on the negative effects induced by chronic exposure of shrimp to deltamethrin at different dietary lipid levels. A feeding experiment of six weeks was carried out to assess whether alterations in dietary lipid levels have an impact on the toxicity of DM. In a feeding experiment on Litopenaeus vannamei, the effects of dietary fat levels on the toxicity of DM were studied. There were six distinct diets created comprising three levels of DM (0.2 mg⋅kg–1, 1 mg⋅kg–1, 5 mg⋅kg–1), and two lipid levels (6.96 %, 10.88 %). The diets were designated as LF0.2, LF1, LF5, HF0.2, HF1, HF5. The growth performance and whole shrimp body lipid were reduced with the increase of DM addition to the diet, and DM caused abnormal changes in lipoproteins (LDL, HDL, LPS) in shrimp when feeding diets containing high doses of DM. Furthermore, GOT, GPT, AKP, and ACP activities were found to be significantly increased by long-term exposure to DM. Meanwhile, the way that genes linked to the nuclear factor kappa-B immune signaling pathway showed a significant increase in the hepatopancreas (dorsal, imd, pelle, ikkβ), intestine (imd, tube, pelle), and muscle (toll, imd, pelle) of shrimp following exposure to DM. Similarly, cellular autophagy genes in the hepatopancreas (atg9, atg12), muscle (atg3, atg9), and intestine (atg3, atg5, atg9, beclin, atg13) were significantly upregulated in a dose-dependent manner after shrimp chronic exposure to DM. Histopathological damage was also induced in the muscles under DM exposure. In summary, chronic exposure to DM resulted in a slowing of growth performance, disruption of lipoprotein metabolism, impairment of hepatopancreatic, intestinal, and muscle-related immune functions, as well as the promotion of autophagy and damage to shrimp muscle.

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Journal of hazardous materials advances
Journal of hazardous materials advances Environmental Engineering
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