Zhang Lang, Zhou Yuntao, Song Ziwei, Liang Hongwei, Zhong Shan, Yu Yali, Liu Ting, Sha Hang, He Li, Gan Jinhua
Yangtze River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Wuhan 430223, China.
Department of Genetics, Wuhan University, Wuhan 430071, China.
Antioxidants (Basel). 2022 Sep 29;11(10):1944. doi: 10.3390/antiox11101944.
As one of the most toxic elements, mercury (Hg) is a widespread toxicant in aquatic environments. Crayfish are considered suitable for indicating the impact of heavy metals on aquatic crustaceans. Nevertheless, Hg toxicity on is largely unknown. In this research, the acute Hg-induced alterations of biochemical responses, histopathology, hepatopancreatic transcriptome, and intestinal microbiome of were studied. Firstly, Hg induced significant changes in reactive oxygen species (ROS) and malonaldehyde (MDA) content as well as antioxidant enzyme activity. Secondly, Hg exposure caused structural damage to the hepatopancreas (e.g., vacuolization of the epithelium and dilatation of the lumen) as well as to the intestines (e.g., dysregulation of lamina epithelialises and extension of lamina proprias). Thirdly, after treatment with three different concentrations of Hg, RNA-seq assays of the hepatopancreas revealed a large number of differentially expressed genes (DEGs) linked to a specific function. Among the DEGs, a lot of redox metabolism- (e.g., ACOX3, SMOX, GPX3, GLO1, and P4HA1), ion transport- (e.g., MICU3, MCTP, PYX, STEAP3, and SLC30A2), drug metabolism- (e.g., HSP70, HSP90A, CYP2L1, and CYP9E2), immune response- (e.g., SMAD4, HDAC1, and DUOX), and apoptosis-related genes (e.g., CTSL, CASP7, and BIRC2) were identified, which suggests that Hg exposure may perturb the redox equilibrium, disrupt the ion homeostasis, weaken immune response and ability, and cause apoptosis. Fourthly, bacterial 16S rRNA gene sequencing showed that Hg exposure decreased bacterial diversity and dysregulated intestinal microbiome composition. At the phylum level, there was a marked decrease in and an increase in after exposure to high levels of Hg. With regards to genus, abundances of , , and were markedly dysregulated after Hg exposures. Our findings elucidate the mechanisms involved in Hg-mediated toxicity in aquatic crustaceans at the tissue, cellular, molecular as well as microbial levels.
作为毒性最强的元素之一，汞（Hg）是水生环境中广泛存在的有毒物质。小龙虾被认为适合用于指示重金属对水生甲壳类动物的影响。然而，汞对小龙虾的毒性在很大程度上尚不清楚。在本研究中，对汞急性诱导的小龙虾生化反应、组织病理学、肝胰腺转录组和肠道微生物群的变化进行了研究。首先，汞诱导活性氧（ROS）和丙二醛（MDA）含量以及抗氧化酶活性发生显著变化。其次，汞暴露导致肝胰腺（如上皮细胞空泡化和管腔扩张）以及肠道（如板层上皮失调和固有层延伸）的结构损伤。第三，用三种不同浓度的汞处理后，肝胰腺的RNA测序分析揭示了大量与特定功能相关的差异表达基因（DEG）。在这些差异表达基因中，鉴定出许多与氧化还原代谢（如ACOX3、SMOX、GPX3、GLO1和P4HA1）、离子转运（如MICU3、MCTP、PYX、STEAP3和SLC30A2）、药物代谢（如HSP70、HSP90A、CYP2L1和CYP9E2）、免疫反应（如SMAD4、HDAC1和DUOX）以及凋亡相关的基因（如CTSL、CASP7和BIRC2），这表明汞暴露可能扰乱氧化还原平衡、破坏离子稳态、削弱免疫反应和能力并导致细胞凋亡。第四，细菌16S rRNA基因测序表明，汞暴露降低了细菌多样性并使肠道微生物群组成失调。在门水平上，暴露于高浓度汞后，变形菌门显著减少，厚壁菌门增加。在属水平上，汞暴露后，气单胞菌属、拟杆菌属和弧菌属的丰度明显失调。我们的研究结果阐明了汞在组织、细胞、分子以及微生物水平上介导的水生甲壳类动物毒性的相关机制。
