Eid Refaat A, Al-Shraim Mubarak, Zaki Mohamed Sa, Kamar Samaa S, Abdel Latif Noha S, Negm Sally, Al-Ani Bahjat, Haidara Mohamed A
Departments of Pathology, College of Medicine, King Khalid University, Abha, Saudi Arabia.
Departments of Anatomy, College of Medicine, King Khalid University, Abha, Saudi Arabia.
Ultrastruct Pathol. 2019;43(4-5):199-208. doi: 10.1080/01913123.2019.1673860. Epub 2019 Oct 10.
Food additives such as nitrates and nitrites, and monosodium glutamate (MSG) used in the food industry increase the risk of certain cancers and inflict damage to vital organs. We sought to determine whether the antioxidant vitamin E can protect against liver injuries induced by a toxic dose of MSG in a rat model of MSG-induced acute liver injury. The model group of rats received a daily dose of MSG (4 gm/kg) for 7 days, whereas the protective groups were either received a 100 mg/kg vitamin E plus MSG or 300 mg/kg vitamin E plus MSG for 7 days. Rats were then sacrificed at day 8. Transmission and light microscopy images revealed substantial liver tissue damage induced by MSG in the model group as demonstrated by apoptotic hepatocytes with Pyknotic nuclei and irregular nuclear membrane, and cytoplasm displayed many vacuoles, swollen mitochondria, dilated endoplasmic reticulum, dilated blood sinusoids and bundles of collagen fibers in extracellular space. Treatment of the model group with vitamin E showed a substantial protection of liver tissue and hepatocellular architecture by 300 mg/kg vitamin E compared to a partial protection by 100 mg/kg vitamin E. In addition, MSG significantly ( < .05) modulated serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD), and glutathione peroxidase (GPx), which were significantly ( < .05) protected with vitamin E. Thus, vitamin E at 300 mg/kg effectively protects against MSG-induced acute liver injury in rats, possibly via the inhibition of inflammation, and up-regulation of endogenous antioxidants.
食品工业中使用的硝酸盐、亚硝酸盐和味精等食品添加剂会增加某些癌症的风险，并对重要器官造成损害。我们试图确定抗氧化剂维生素E是否能在味精诱导的急性肝损伤大鼠模型中，预防由毒性剂量的味精引起的肝损伤。模型组大鼠每天接受一剂味精（4克/千克），持续7天，而保护组则分别接受100毫克/千克维生素E加味精或300毫克/千克维生素E加味精，持续7天。然后在第8天处死大鼠。透射和光学显微镜图像显示，模型组中味精诱导了严重的肝组织损伤，表现为凋亡的肝细胞，细胞核固缩，核膜不规则，细胞质出现许多空泡、线粒体肿胀、内质网扩张、血窦扩张以及细胞外空间有胶原纤维束。与100毫克/千克维生素E的部分保护作用相比，用300毫克/千克维生素E治疗模型组显示出对肝组织和肝细胞结构的显著保护。此外，味精显著（<0.05）调节了血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）的水平，而维生素E对这些指标有显著（<0.05）的保护作用。因此，300毫克/千克的维生素E能有效预防大鼠味精诱导的急性肝损伤，可能是通过抑制炎症和上调内源性抗氧化剂来实现的。
