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慢性水基锌暴露对凡纳滨对虾肝胰腺的毒性。

Toxicity of chronic waterborne zinc exposure in the hepatopancreas of white shrimp Litopenaeus vannamei.

机构信息

College of Fisheries, Guangdong Ocean University, Zhanjiang, 524025, PR China; Guangdong Provincial Key Laboratory of Pathogenic Biology and Epidemiology for Aquatic Economic Animals & Key Laboratory of Control for Diseases of Aquatic Economic Animals of Guangdong Higher Education Institutes, Zhanjiang, 524025, PR China.

College of Fisheries, Guangdong Ocean University, Zhanjiang, 524025, PR China; Key Laboratory of Aquatic, Livestock and Poultry Feed Science and Technology in South China, Ministry of Agriculture, Zhanjiang, 524025, PR China; Aquatic Animals Precision Nutrition and High Efficiency Feed Engineering Research Center of Guangdong Province, Zhanjiang, China.

出版信息

Chemosphere. 2022 Dec;309(Pt 1):136553. doi: 10.1016/j.chemosphere.2022.136553. Epub 2022 Sep 22.

DOI:10.1016/j.chemosphere.2022.136553
PMID:36155019
Abstract

Zinc (Zn) is necessary for the survival of aquatic organisms; nevertheless, the accumulation of Zn in excessive amounts may have toxic consequences. Few studies focusing on the biochemical, morphological, and transcriptional effects of aqueous Zn in Litopenaeus vannamei have been reported, and the underlying toxic mechanism remains largely unknown. The present study was performed to investigate the growth performance, morphological alterations, physiological changes, and transcriptional responses after Zn exposure at 0 (control), 0.01, 0.1, and 1 mg/L concentrations for 30 days in white shrimp L. vannamei hepatopancreas. The results found that survival rate (SR) and growth performance were significantly reduced in 1 mg/L Zn group. Significant structural damage and significant Zn accumulation in hepatopancreas were observed. The activities of trypsin and amylase (AMS), and the total antioxidant capacity (T-AOC) were attenuated, while the production of reactive oxygen species (ROS) and malondialdehyde (MDA) content were significantly increased after Zn exposure. Many differentially expressed genes (DEGs) were obtained after Zn exposure, and the majority of these DEGs were downregulated. Ten DEGs involved in oxidative stress, immunological response, apoptosis, and other processes were selected for qRT-PCR validation and the expression profiles of these DEGs kept well consistent with the transcriptome data, which confirmed the accuracy and reliability of the transcriptome results. Subsequently, we screened 12 genes to examine the changes of expression in different concentrations in more detail. All the results implying that Zn exposure caused severe histopathological changes and increased Zn accumulation in hepatopancreas, altered immune, antioxidant and detoxifying response by regulating the gene expressions of related genes, and eventually might trigger apoptosis. These findings provide valuable information and a new perspective on the molecular toxicity of crustaceans in response to environmental heavy metal exposure.

摘要

锌(Zn)是水生生物生存所必需的;然而,过量积累 Zn 可能会产生毒性后果。目前,关于 Zn 在凡纳滨对虾(Litopenaeus vannamei)中的生化、形态和转录影响的研究较少,其潜在的毒性机制在很大程度上尚不清楚。本研究旨在探讨在 0(对照)、0.01、0.1 和 1 mg/L Zn 暴露 30 天后,凡纳滨对虾肝胰腺中的生长性能、形态变化、生理变化和转录反应。结果发现,1 mg/L Zn 组的存活率(SR)和生长性能显著降低。观察到肝胰腺结构损伤和 Zn 积累显著。暴露于 Zn 后,胰蛋白酶和淀粉酶(AMS)的活性以及总抗氧化能力(T-AOC)降低,而活性氧(ROS)的产生和丙二醛(MDA)含量显著增加。暴露于 Zn 后获得了许多差异表达基因(DEGs),其中大多数基因下调。选择了 10 个与氧化应激、免疫反应、细胞凋亡等过程相关的 DEGs 进行 qRT-PCR 验证,这些 DEGs 的表达谱与转录组数据保持很好的一致性,证实了转录组结果的准确性和可靠性。随后,我们筛选了 12 个基因,以更详细地研究不同浓度下表达的变化。所有结果表明,Zn 暴露导致肝胰腺组织发生严重的组织病理学变化和 Zn 积累增加,通过调节相关基因的表达,改变了免疫、抗氧化和解毒反应,最终可能引发细胞凋亡。这些发现为甲壳类动物对环境重金属暴露的分子毒性提供了有价值的信息和新视角。

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