Cadmium (Cd) is a threatening heavy metal pollutant to aquatic organisms. The hepatopancreas plays a crucial role in combating environmental stress and enhancing the immune defense of aquatic species. The exact mechanism behind the damage induced by Cadmium in the hepatopancreas of is unclear. Thus, this study aimed to elucidate the potential mechanisms of Cadmium's impact on the hepatopancreas of through physiological, histological, and transcriptomic analyses. After 72 h of exposure to the 0.5 mg/L concentration of cadmium results in the reduction of superoxide dismutase and catalase activities, coupled with an increase in hydrogen peroxide and malondialdehyde levels, which leads to damage in both the gills and hepatopancreas. This causes severe histological changes in the gills and hepatopancreas of , characterized by irregularities in the gill filaments and ruptures in the basal membrane of the hepatopancreas. Comparative transcriptomic analysis of revealed the upregulation of several genes associated with pathways related to metabolism (ko01100), antigen processing and presentation (ko04612), and cell apoptosis (ko04215), indicating adaptive response mechanisms to Cadmium exposure. Transcriptomic analysis also showed that Cadmium exposure induced the expression of genes related to detoxification and apoptosis, such as heat shock proteins, metallothionein, and , suggesting adverse effects on the normal physiological functions of . Our study provides comprehensive insights into the toxicological mechanisms and impacts of Cadmium on

中文翻译：

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镉诱导的墨吉明对虾肝胰腺氧化应激、组织病理学和转录组变化

镉（Cd）是一种对水生生物有威胁的重金属污染物。肝胰腺在对抗环境压力和增强水生物种的免疫防御方面发挥着至关重要的作用。镉对肝胰腺造成损害的确切机制尚不清楚。因此，本研究旨在通过生理、组织学和转录组分析来阐明镉对肝胰腺影响的潜在机制。暴露于0.5 mg/L浓度的镉72小时后，超氧化物歧化酶和过氧化氢酶活性降低，同时过氧化氢和丙二醛水平增加，从而导致鳃和肝胰腺受损。这会导致鳃和肝胰腺发生严重的组织学变化，其特征是鳃丝不规则和肝胰腺基底膜破裂。比较转录组分析揭示了与代谢 (ko01100)、抗原加工和呈递 (ko04612) 以及细胞凋亡 (ko04215) 相关途径相关的几个基因的上调，表明对镉暴露的适应性反应机制。转录组分析还表明，镉暴露诱导了与解毒和凋亡相关的基因表达，如热休克蛋白、金属硫蛋白等，这表明对镉的正常生理功能产生不利影响。我们的研究为镉的毒理学机制和影响提供了全面的见解