Zhao Junqiang, Chen Jianqiang, Tian Xiuhui, Jiang Lisheng, Cui Qingkui, Sun Yanqing, Wu Ningning, Liu Ge, Ding Yuzhu, Wang Jing, Liu Yongchun, Han Dianfeng, Xu Yingjiang
Yantai Key Laboratory of Quality and Safety Control and Deep Processing of Marine Food, Shandong Key Laboratory of Marine Ecological Restoration, Shandong Marine Resource and Environment Research Institute, Yantai 264006, China.
School of Food, Shanghai Ocean University, Shanghai 200120, China.
Toxics. 2023 Feb 27;11(3):226. doi: 10.3390/toxics11030226.
Amantadine exposure can alter biological processes in sea cucumbers, which are an economically important seafood in China. In this study, amantadine toxicity in was analyzed by oxidative stress and histopathological methods. Quantitative tandem mass tag labeling was used to examine changes in protein contents and metabolic pathways in intestinal tissues after exposure to 100 µg/L amantadine for 96 h. Catalase activity significantly increased from days 1 to 3 of exposure, but it decreased on day 4. Superoxide dismutase and glutathione activities were inhibited throughout the exposure period. Malondialdehyde contents increased on days 1 and 4 but decreased on days 2 and 3. Proteomics analysis revealed 111 differentially expressed proteins in the intestines of after amantadine exposure compared with the control group. An analysis of the involved metabolic pathways showed that the glycolytic and glycogenic pathways may have increased energy production and conversion in after amantadine exposure. The NF-κB, TNF, and IL-17 pathways were likely induced by amantadine exposure, thereby activating NF-κB and triggering intestinal inflammation and apoptosis. Amino acid metabolism analysis showed that the leucine and isoleucine degradation pathways and the phenylalanine metabolic pathway inhibited protein synthesis and growth in This study investigated the regulatory response mechanisms in intestinal tissues after exposure to amantadine, providing a theoretical basis for further research on amantadine toxicity.
金刚烷胺暴露会改变海参体内的生物过程，海参是中国一种具有重要经济价值的海产品。在本研究中，通过氧化应激和组织病理学方法分析了金刚烷胺对海参的毒性。采用定量串联质量标签标记法，检测了海参肠道组织在暴露于100μg/L金刚烷胺96小时后蛋白质含量和代谢途径的变化。过氧化氢酶活性在暴露的第1天至第3天显著增加，但在第4天下降。超氧化物歧化酶和谷胱甘肽活性在整个暴露期间均受到抑制。丙二醛含量在第1天和第4天增加，但在第2天和第3天下降。蛋白质组学分析显示，与对照组相比，金刚烷胺暴露后海参肠道中有111种差异表达蛋白。对所涉及代谢途径的分析表明，金刚烷胺暴露后，糖酵解和糖原生成途径可能增加了海参的能量产生和转化。NF-κB、TNF和IL-17途径可能因金刚烷胺暴露而被诱导，从而激活NF-κB并引发肠道炎症和细胞凋亡。氨基酸代谢分析表明，亮氨酸和异亮氨酸降解途径以及苯丙氨酸代谢途径抑制了海参的蛋白质合成和生长。本研究探讨了海参肠道组织暴露于金刚烷胺后的调节反应机制，为进一步研究金刚烷胺毒性提供了理论依据。
