Animal Wealth Development Department, Faculty of Veterinary Medicine, Zagazig University, Zagazig, Egypt.
Forensic Medicine and Toxicology, Department, Faculty of Veterinary Medicine, Zagazig University, 44511 Zagazig, Egypt.
Ecotoxicol Environ Saf. 2018 Oct 30;162:235-244. doi: 10.1016/j.ecoenv.2018.07.003. Epub 2018 Jul 11.
In this study, we aimed to assess the differential toxic impact, induced by furan exposure, on the liver and kidney tissues by estimating reactive oxygen species (ROS) level, total antioxidant capacity (TAC), oxidative damage, and the tissue injury markers in a male rat model. To explain such impacts, 20 rats were assigned into two groups: a control group, where rats were administered corn oil as a vehicle, and a furan-administered group, where furan was orally administered to rats at a dose of 16 mg/kg b wt/day (five days per week over eight weeks). The transcriptional levels of intermediate filament proteins (desmin, vimentin, nestin, and connexin 43) were assessed by using quantitative real-time polymerase chain reaction (PCR), and the cell proliferation markers (proliferating cell nuclear antigen [PCNA] and proliferation-associated nuclear antigen [Ki-67]) were recognized by immunohistochemical analysis. Furthermore, the ultrastructural changes of liver and kidney were monitored using electron microscopy. Our findings showed that furan exposure could induce hepatic and renal damage to different extents. Furan can increase the ROS content, oxidative damage indices, and liver tissue injury indices but not kidney injury indices. Furthermore, it decreases the TAC in the serum of exposed rats. In addition, furan exposure was associated with changes in the mRNA expression pattern of intermediate filament proteins in both kidney and liver tissues. Moreover, furan enhances the expression of PCNA and Ki-67 in the liver tissues but not in the kidney tissues. The ultrastructure evaluation revealed the incidence of glomerular podocyte degeneration and hepatocyte injury. These results conclusively demonstrate that the deleterious effects of furan are caused by promoting fibrosis and hepatocyte proliferation in liver tissues and triggering podocyte injury in the kidney tissues.
在这项研究中，我们旨在通过评估活性氧 (ROS) 水平、总抗氧化能力 (TAC)、氧化损伤以及雄性大鼠模型中的组织损伤标志物，来评估呋喃暴露对肝脏和肾脏组织的毒性差异。为了解释这些影响，将 20 只大鼠分为两组：对照组，大鼠给予玉米油作为载体；呋喃处理组，大鼠每天口服呋喃 16mg/kg b.wt（每周 5 天，共 8 周）。通过实时定量聚合酶链反应 (PCR) 评估中间丝蛋白（结蛋白、波形蛋白、巢蛋白和连接蛋白 43）的转录水平，并用免疫组织化学分析识别细胞增殖标志物（增殖细胞核抗原 [PCNA] 和增殖相关核抗原 [Ki-67]）。此外，使用电子显微镜监测肝脏和肾脏的超微结构变化。我们的研究结果表明，呋喃暴露可以在不同程度上引起肝和肾损伤。呋喃可以增加 ROS 含量、氧化损伤指标和肝组织损伤指标，但不会增加肾损伤指标。此外，它还降低了暴露大鼠血清中的 TAC。此外，呋喃暴露与肾脏和肝脏组织中中间丝蛋白 mRNA 表达模式的变化有关。此外，呋喃增强了肝组织中 PCNA 和 Ki-67 的表达，但在肾组织中没有。超微结构评估显示肾小球足细胞退化和肝细胞损伤的发生率。这些结果表明，呋喃的有害影响是通过促进肝组织中的纤维化和肝细胞增殖以及触发肾组织中的足细胞损伤引起的。
