Department of Animal and Environmental Biology, Faculty of Life Sciences, University of Benin, Benin City, Nigeria.
Unit for Environmental Sciences and Management, North-West University, Private Bag X6001, Potchefstroom, 2520, South Africa.
Arch Environ Contam Toxicol. 2021 Feb;80(2):414-425. doi: 10.1007/s00244-020-00792-1. Epub 2021 Jan 1.
The hepatotoxic effects of sub-lethal concentrations of atrazine (2.5, 25, 250, and 500 μg L) on Clarias gariepinus juveniles were assessed for 28 days in a quality-controlled laboratory procedure. The study was designed to determine the effects of atrazine on selected liver function biomarkers: alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), albumin (ALB) and total protein (TP), and to analyze the liver tissues of the fish using a quantitative and qualitative histology-based health assessment protocol. The levels of ALB and TP in exposed specimens were observed to decrease with increasing concentrations of atrazine. However, the activities of ALT, AST, and ALP showed significant (p < 0.05) increase with increasing concentrations of atrazine. Hepatic assessment of the liver tissues revealed marked histopathological alterations, including structural changes (necrotic/apoptotic liver tissue, poor hepatic cord structure, and loss of normal architecture) in 52.2% of the liver tissues in the treatment groups; plasma alterations (vacuolation or fat inclusions, 22.9%) of hepatocytes; hypertrophied hepatocyte (55.2%); nuclear alterations (52.1%); focal necrosis (16.7%); complete degeneration of hepatocytes (60.45%); sinusoids congested with red blood cells or vascular congestion (70.8%); and karyolysis of the nucleus (18.8%). Findings from this study suggest that atrazine interferes with liver function markers and disrupts the normal architectural and structural components of the liver resulting in noninfectious liver injury. This condition resulted in repeated cycles, cell deaths, and inflammation, which could result in the eventual death of the exposed fish if exposure duration was prolonged.
本研究采用质量控制实验室程序，评估了亚致死浓度（2.5、25、250 和 500μg/L）莠去津对罗非鱼幼鱼的肝毒性作用，为期 28 天。该研究旨在确定莠去津对选定的肝功能生物标志物（丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）、碱性磷酸酶（ALP）、白蛋白（ALB）和总蛋白（TP））的影响，并使用定量和定性组织学健康评估方案分析鱼的肝脏组织。结果显示，暴露组的 ALB 和 TP 水平随着莠去津浓度的增加而降低，而 ALT、AST 和 ALP 的活性则随着莠去津浓度的增加而显著增加（p<0.05）。肝组织评估显示，肝脏组织出现明显的组织病理学改变，包括结构改变（坏死/凋亡肝组织、肝索结构不良和正常结构丧失），在处理组的 52.2%的肝脏组织中可见；肝实质细胞的血浆改变（空泡或脂肪内含物，22.9%）；肥大的肝细胞（55.2%）；核改变（52.1%）；局灶性坏死（16.7%）；肝细胞完全变性（60.45%）；窦状隙充血伴红细胞或血管充血（70.8%）；核溶解（18.8%）。本研究结果表明，莠去津干扰肝功能标志物，并破坏肝脏的正常结构和组织结构，导致非传染性肝损伤。这种情况导致反复的细胞死亡和炎症，如果暴露时间延长，可能会导致暴露鱼类最终死亡。
