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Hepatotoxic Effects of Atrazine on Clarias gariepinus (Burchell, 1822): Biochemical and Histopathological Studies
Archives of Environmental Contamination and Toxicology ( IF 4 ) Pub Date : 2021-01-01 , DOI: 10.1007/s00244-020-00792-1
P. A. Opute , I. P. Oboh

The hepatotoxic effects of sub-lethal concentrations of atrazine (2.5, 25, 250, and 500 μg L−1) 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.



中文翻译:

阿特拉津对苦Cl的肝毒性作用(Burchell,1822年):生化和组织病理学研究

在质量控制的实验室程序中,评估了亚致死浓度(2.5、25、250和500μgL -1)的亚致死浓度对Cl鱼的肝毒性作用,评估了28天。该研究旨在确定阿特拉津对所选肝功能生物标志物的影响: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),并分析肝脏使用基于组织学的定量和定性健康评估方案对鱼的组织进行分析。观察到暴露样品中ALB和TP的水平随着阿特拉津浓度的增加而降低。但是,ALT,AST和ALP的活性显示出显着的(p <0.05)随阿特拉津浓度的增加而增加。肝组织的肝评估显示,治疗组52.2%的肝组织具有明显的组织病理学改变,包括结构变化(坏死/凋亡的肝组织,肝索结构不良和结构丧失)。肝细胞的血浆改变(空泡或脂肪包裹体,占22.9%);肥大的肝细胞(55.2%); 核变化(52.1%); 局灶性坏死(16.7%); 肝细胞完全变性(60.45%);红细胞充血或血管充血的正弦曲线(70.8%);和核的核解(18.8%)。这项研究的发现表明,at去津会干扰肝功能标志物并破坏正常的肝脏结构和结构成分,从而导致非感染性肝损伤。

更新日期:2021-01-01
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