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Zinc oxide nanoparticles inhibit dimethylnitrosamine induced liver injury in rat
Chemico-Biological Interactions ( IF 5.1 ) Pub Date : 2017-10-10 , DOI: 10.1016/j.cbi.2017.10.009
Varsha Rani , Yeshvandra Verma , Kavita Rana , Suresh Vir Singh Rana

Dimethylnitrosamine (DMN) is a potent hepatotoxic, carcinogenic and mutagenic compound. It induces massive liver cell necrosis and death in experimental animals. Several drugs have been tested in the past for their protective behavior against DMN toxicity. However, it is for the first time that therapeutic intervention of ZnONPs (zinc oxide nanoparticles) has been studied against its toxicity. Present results show that a post treatment of ZnONPs (50 mg/kg) to DMN (2 μl/100 g body weight) treated rats reduces lipid peroxidation, oxidative stress and fibrosis in the liver. It diminishes serum ALT (alanine transaminases), AST (aspartate transaminases) and LDH (lactate dehydrogenase) showing improvement in liver function. Reduced values of proinflammatory cytokines viz. TNF-α and IL-12 also support its protective effects. Histopathological observations also indicate improvement in liver cell morphology. It is postulated that ZnONPs offer protection through selective toxicity to proliferating tissue including adenomatous islands formed in the liver. Zinc metallothionein (Zn-MT) induced by ZnONPs may also contribute in the amelioration of DMN induced toxic effects. Diminution of oxidative stress by ZnONPs remains to be the key mechanism involved in its protective effects. However, toxicity of ZnONPs in the liver needs to be monitored simultaneously.



中文翻译:

氧化锌纳米颗粒抑制二甲基亚硝胺诱导的大鼠肝损伤

二甲基亚硝胺(DMN)是有效的肝毒性,致癌性和致突变性化合物。它在实验动物中引起大量肝细胞坏死和死亡。过去已经测试了几种药物对DMN毒性的保护作用。然而,这是首次针对其毒性研究了ZnONPs(氧化锌纳米粒子)的治疗性干预。目前的结果表明,将ZnONPs(50 mg / kg)后处理为DMN(2μl/ 100 g体重)处理的大鼠,可以减少肝脏中的脂质过氧化,氧化应激和纤维化。它会降低血清ALT(丙氨酸转氨酶),AST(天冬氨酸转氨酶)和LDH(乳酸脱氢酶),从而改善肝功能。降低促炎细胞因子的价值,即。TNF-α和IL-12也支持其保护作用。组织病理学观察还表明肝细胞形态有所改善。据推测,ZnONPs通过对包括肝脏中形成的腺瘤岛在内的增生组织的选择性毒性来提供保护。ZnONPs诱导的金属硫蛋白锌(Zn-MT)也可能有助于DMN诱导的毒性作用的改善。ZnONP减轻氧化应激仍然是其保护作用的关键机制。但是,需要同时监测ZnONP在肝脏中的毒性。ZnONP减轻氧化应激仍然是其保护作用的关键机制。但是,需要同时监测ZnONP在肝脏中的毒性。ZnONP减轻氧化应激仍然是其保护作用的关键机制。但是,ZnONPs在肝脏中的毒性需要同时进行监测。

更新日期:2017-10-10
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