Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Kafrelsheikh University, Egypt.
Department of Anatomy, Faculty of Medicine, University of Jeddah, Jeddah, Saudi Arabia.
Food Chem Toxicol. 2023 Jun;176:113744. doi: 10.1016/j.fct.2023.113744. Epub 2023 Mar 24.
The terrible reality is that acrylamide (AA) is a common food contaminant found in a wide variety of commonly consumed foods. This research involves the advancement of a more dependable technique for the bio-fabrication of zinc oxide nanoparticles (ZNPs) through the green method using Moringa Oleifera extract (MO-ZNPs) as an efficient chelating agent for acrylamide (AA). The effects of AA on glutathione redox dynamics, liver function, lipid profile, and zinc residues in Sprague Dawley rats are investigated. Finally, the microarchitecture and immunohistochemical staining of Caspase-3 and CYP2E1 were determined in the liver tissue of rats. Four separate groups, including control, MO-ZNPs (10 mg/kg b. wt), AA (20 mg/kg b. wt), and AA + MO-ZNPs for 60 days. The results revealed a suppressed activity of glutathione redox enzymes (GSH, GPX,and GSR) on both molecular and biochemical levels. Also, AA caused elevated liver enzymes, hepatosomatic index, and immunohistochemical staining of caspase-3 and CYP2E1 expression. MO-ZNPs co-treatment, on the other hand, stabilized glutathione-related enzyme gene expression, normalized hepatocellular enzyme levels, and restored hepatic tissue microarchitectures. It could be assumed that MO-ZNPs is a promising hepatoprotective molecule for alleviating AA-induced hepatotoxicity. We witnessed changes in glutathione redox dynamics to be restorative. Glutathione and cytochrome P450 2E1 play crucial roles in AA detoxification, so maintaining a healthy glutathione redox cycle is necessary for disposing of AA toxicity.
可怕的现实是,丙烯酰胺(AA)是一种常见的食物污染物,存在于各种常见的食用食品中。本研究涉及通过绿色方法使用辣木提取物(MO-ZNPs)作为丙烯酰胺(AA)的有效螯合剂,来推进更可靠的氧化锌纳米粒子(ZNPs)的生物制造技术。研究了 AA 对谷胱甘肽氧化还原动力学、肝功能、脂质谱和 Sprague Dawley 大鼠中锌残留的影响。最后,确定了大鼠肝组织中 Caspase-3 和 CYP2E1 的微观结构和免疫组织化学染色。包括对照组、MO-ZNPs(10 mg/kg b.wt)、AA(20 mg/kg b.wt)和 AA+MO-ZNPs 在内的四个独立组,持续 60 天。结果表明,谷胱甘肽氧化还原酶(GSH、GPX 和 GSR)的活性在分子和生化水平上均受到抑制。此外,AA 导致肝酶升高、肝体比升高和 caspase-3 和 CYP2E1 表达的免疫组织化学染色增加。另一方面,MO-ZNPs 共同处理稳定了谷胱甘肽相关酶基因的表达,使肝细胞酶水平正常化,并恢复了肝组织的微观结构。可以假设 MO-ZNPs 是一种有前途的肝保护分子,可减轻 AA 诱导的肝毒性。我们观察到谷胱甘肽氧化还原动力学的变化是恢复性的。谷胱甘肽和细胞色素 P450 2E1 在 AA 解毒中起关键作用,因此保持健康的谷胱甘肽氧化还原循环对于处理 AA 毒性是必要的。