PDF(Pubmed)
Abstract：
Water bodies are highly pollution-prone areas in which mercury (Hg) is considered as a major menace to aquatic organisms. However, the information about the toxicity of mercuric chloride (HgCl2) in a vital organ such as the liver of fish is still inadequate. This study aimed to assess the impact of mercuric chloride (HgCl2) exposure on the liver of Channa punctata fish over 15, 30, and 45 days, at two different concentrations (0.039 mg/L and 0.078 mg/L). Mercury is known to be a significant threat to aquatic life, and yet, information regarding its effects on fish liver remains limited. The results of this study demonstrate that exposure to HgCl2 significantly increases oxidative stress markers, such as lipid peroxidation (LPO) and protein carbonyls (PC), as well as the levels of serum glutamic-oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) in the fish. Additionally, the transcriptional and protein analysis of specific genes and molecules associated with necroptosis and inflammation, such as ABCG2, TNF α, Caspase 3, RIPK 3, IL-1β, Caspase-1, IL-18, and RIPK1, confirm the occurrence of necroptosis and inflammation in the liver. Histopathological and ultrastructural examinations of the liver tissue further reveal a significant presence of liver steatosis. Interestingly, the upregulation of PPARα suggests that the fish\'s body is actively responding to counteract the effects of liver steatosis. This study provides a comprehensive analysis of oxidative stress, biochemical changes, gene expression, protein profiles, and histological findings in the liver tissue of fish exposed to mercury pollution in freshwater environments.
摘要：
水体是极易污染的地区，汞（Hg）被认为是对水生生物的主要威胁。然而,关于氯化汞（HgCl2）在鱼类肝脏等重要器官中的毒性的信息仍然不足。本研究旨在评估氯化汞（HgCl2）暴露在15、30和45天内对Channapunctata鱼肝脏的影响，在两个不同的浓度（0.039mg/L和0.078mg/L）。众所周知，汞对水生生物是一个重大威胁，然而，有关其对鱼肝影响的信息仍然有限。这项研究的结果表明，暴露于HgCl2显着增加氧化应激标志物，如脂质过氧化(LPO)和蛋白质羰基(PC)，以及鱼的血清谷草转氨酶（SGOT）和血清谷丙转氨酶（SGPT）的水平。此外,与坏死和炎症相关的特定基因和分子的转录和蛋白质分析，如ABCG2，TNFα，Caspase3,RIPK3,IL-1β,Caspase-1，IL-18和RIPK1证实了肝脏中坏死和炎症的发生。肝组织的组织病理学和超微结构检查进一步揭示了肝脏脂肪变性的显著存在。有趣的是,PPARα的上调表明鱼体正在积极反应以抵消肝脏脂肪变性的影响。本研究提供了一个全面的分析氧化应激，生化变化，基因表达，蛋白质谱,以及在淡水环境中暴露于汞污染的鱼类肝脏组织的组织学发现。
