首页> 美国卫生研究院文献>Heliyon >Ameliorating effect of melatonin on mercuric chloride-induced neurotoxicity in rats
【2h】

Ameliorating effect of melatonin on mercuric chloride-induced neurotoxicity in rats

机译:褪黑素对大鼠氯化汞诱导神经毒性的改善作用

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Mercury is a highly toxic metal. It induces its toxicity via production of reactive oxygen species. Brain tissues are more susceptible to oxidative damage. Melatonin and its metabolites are free radical scavengers. The aim of this work is to elucidate the neuroprotective effect of melatonin on mercuric chloride-induced neurotoxicity in rats. Fifty male albino rats were used and divided into five groups. Group I acts as normal control. Group II (LD HgCl2) received mercuric chloride at a dose of 2 mg/kg. Group III (HD HgCl2) received HgCl2 at a dose of 4 mg/kg. Rats in group IV (LD HgCl2 +MLT) received HgCl2 2 mg/kg + Melatonin 5 mg/kg. Rats in group V (HD HgCl2+MLT) received HgCl2 4 mg/kg + Melatonin5 mg/kg. This study revealed that mercuric chloride decreased the activity of superoxide dismutase, catalase and glutathione peroxidase enzymes and increased malondialdehyde levels. Toxicity of mercuric chloride lead to upregulation of the gene expression level vascular endothelial growth factor. HgCl2 induced fragmentation of rough endoplasmic reticulum, ballooning of Golgi apparatus, nuclear and cytoplasmic degeneration of pyramidal neurones of rat cerebral cortex. This neuronal damage caused by HgCl2 was significantly improved by melatonin.
机译:汞是一种剧毒的金属。它通过生产活性氧物种诱导其毒性。脑组织更容易受到氧化损伤的影响。褪黑激素及其代谢物是自由基清除剂。这项工作的目的是阐明褪黑素对大鼠氯化酰氯诱导的神经毒性的神经保护作用。使用50只雄性白化大鼠并分为五组。小组充当正常控制。 II组(LD HGCL2)以2mg / kg的剂量接收酰氯酰氯。 III组(HD HGCL2)以4mg / kg的剂量接受HgCl2。第IV组大鼠(LD HGCL2 + MLT)接受HGCl 2 2mg / kg +褪黑素5mg / kg。对V(HD HGCL2 + MLT)的大鼠接受HGCl 2 4mg / kg +褪黑素5mg / kg。该研究表明,氯化汞降低了超氧化物歧化酶,过氧化氢酶和谷胱甘肽过氧化物酶的活性和丙二醛水平的增加。氯化汞的毒性导致基因表达水平血管内皮生长因子的上调。 HGCL2诱导粗糙内质网的碎裂,Golgi装置的膨胀,大鼠脑皮层的金字塔神经元的核和细胞质变性。褪黑激素显着​​改善了由HGCL2引起的这种神经元损伤。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号