Wuxi Fisheries College, Nanjing Agricultural University, Wuxi 214081, China; Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.
Wuxi Fisheries College, Nanjing Agricultural University, Wuxi 214081, China; Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.
Sci Total Environ. 2024 Mar 20;917:170393. doi: 10.1016/j.scitotenv.2024.170393. Epub 2024 Jan 26.
Hydrogen peroxide (HO), a prevalent reactive oxygen species (ROS) found in natural aquatic environments, has garnered significant attention for its potential toxicity in fish. However, the molecular mechanisms underlying this toxicity are not yet comprehensively understood. This study aimed to assess HO-induced liver dysfunction in common carp (Cyprinus carpio) and elucidate the underlying molecular mechanisms via biochemical and transcriptomic analyses. Common carp were divided into normal control (NC) and HO-treated groups (1 mM HO), the latter of which was exposed to HO for 1 h per day over a period of 14 days. Serum biochemical analyses indicated that exposure to HO resulted in moderate liver damage, characterized by elevated alanine aminotransferase (ALT) activity and lowered albumin (Alb) level. Concurrently, HO exposure induced oxidative stress and modified the hepatic metabolic enzyme levels. Transcriptome analysis highlighted that 1358 and 1188 genes were significantly downregulated and upregulated, respectively, in the HO-treated group. These differentially expressed genes (DEGs) were significantly enriched in protein synthesis and a variety of metabolic functions such as peptide biosynthetic processes, protein transport, ribonucleoprotein complex biogenesis, oxoacid metabolic processes, and tricarboxylic acid metabolic processes. Dysregulation of protein synthesis is principally associated with the downregulation of three specific pathways: ribosome biogenesis, protein export, and protein processing in the endoplasmic reticulum (ER). Furthermore, metabolic abnormalities were primarily characterized by inhibition of the citrate cycle (TCA) and fatty acid biosynthesis. Significantly, anomalies in both protein synthesis and metabolic function may be linked to aberrant regulation of the insulin signaling pathway. These findings offer innovative insights into the mechanisms underlying HO toxicity in aquatic animals, contributing to the assessment of ecological risks.
过氧化氢（HO）是天然水生环境中普遍存在的一种活性氧（ROS），因其对鱼类的潜在毒性而受到广泛关注。然而，其毒性的分子机制尚不完全清楚。本研究旨在评估过氧化氢（HO）诱导的鲤鱼（Cyprinus carpio）肝损伤，并通过生化和转录组分析阐明其潜在的分子机制。将鲤鱼分为正常对照组（NC）和 HO 处理组（1 mM HO），后者每天暴露于 HO 中 1 小时，持续 14 天。血清生化分析表明，暴露于 HO 会导致中等程度的肝损伤，表现为丙氨酸氨基转移酶（ALT）活性升高和白蛋白（Alb）水平降低。同时，HO 暴露诱导氧化应激并改变了肝脏代谢酶水平。转录组分析表明，HO 处理组中有 1358 个基因显著下调，1188 个基因显著上调。这些差异表达基因（DEGs）在蛋白质合成和各种代谢功能中显著富集，如肽生物合成过程、蛋白质运输、核糖核蛋白复合物生物发生、氧化酸代谢过程和三羧酸代谢过程。蛋白质合成的失调主要与核糖体生物发生、蛋白质输出和内质网（ER）中蛋白质加工的三个特定途径的下调有关。此外，代谢异常主要表现为柠檬酸循环（TCA）和脂肪酸生物合成的抑制。值得注意的是，蛋白质合成和代谢功能的异常可能与胰岛素信号通路的异常调节有关。这些发现为水生动物 HO 毒性的机制提供了新的见解，有助于评估生态风险。
