Selenium Effects on Oxidative Stress-Induced Calcium Signaling Pathways in Parkinson’s Disease

被引：0
作者：
Sanaz Salaramoli
Hamidreza Joshaghani
Seyed Isaac Hashemy
机构：
[1] Mashhad University of Medical Sciences,Student Research Committee, Faculty of Medicine
[2] Mashhad University of Medical Sciences,Department of Clinical Biochemistry, Faculty of Medicine
[3] Golestan University of Medical Sciences,Laboratory Sciences Research Center
[4] Mashhad University of Medical Sciences,Surgical Oncology Research Center
来源：
Indian Journal of Clinical Biochemistry | 2022年 / 37卷
关键词：
Parkinson's disease; Calcium signaling; Selenium; Oxidative stress; Glutathione peroxidase (GPX);
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Parkinson’s disease (PD) is a neurological disorder in which oxidative stress and reactive oxygen species productions are proposed to be involved in its pathogenesis. Despite considerable advancement in Selenium’s (Se) molecular biology and metabolism, we do not know much about the cell type-specific pattern of Se distribution in the brain of PD humans and experimental animals. Although, there is plenty of evidence around the role of Se deficiency in PD’s pathogenesis impacting lipid peroxidation and reducing glutathione (GSH) and glutathione peroxidase (GPX). It has been suggested that Se has an inducible role in selenium-dependent GPX activity in PD animals and humans. However, calcium as a second messenger regulates the neuron cells’ essential activities, but its overloading leads to cellular oxidative stress and apoptosis. Therefore, Se’s antioxidant role can affect calcium signaling and alleviate its complications. There are signs of Se and Selenoproteins incorporation in protecting stress oxidative in various pathways. In conclusion, there is convincing proof for the crucial role of Se and Calcium in PD pathogenesis.
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页码：257 / 266
页数：9
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