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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/43577

Title: Taurine resumed neuronal differentiation in arsenite-treated N2a cells through reducing oxidative stress, endoplasmic reticulum stress, and mitochondrial dysfunction
Authors: Chien‑Te Chou;Hong‑Ting Lin;Pai‑An Hwang;Shang‑Ta Wang;Cheng‑Hong Hsieh;Deng‑Fwu Hwang
Contributors: 國立臺灣海洋大學:生命科學系
Keywords: Arsenite;Neuronal differentiation;Taurine;ER stress;Oxidative stress
Date: 2014-12-30
Issue Date: 2017-10-05T07:17:22Z
Publisher: Amino Acids
Abstract: Abstract:The goal of the study is to investigate the preventive effect of taurine against arsenite-induced arrest of neuronal differentiation in N2a cells. Our results revealed that taurine reinstated the neurite outgrowth in arsenite-treated N2a cells. Meanwhile, arsenite-induced oxidative stress and mitochondrial dysfunction as well as degradation of mitochondria DNA (mtDNA) were also inhibited by co-treatment of taurine. Since oxidative stress and mitochondrial dysfunction is closely associated with endoplasmic reticulum (ER) stress, we further examined indicators of ER stress, 78 kDa glucose-regulated protein (GRP78), and C/EBP-homologous protein (CHOP) protein expression. The results demonstrated that taurine significantly reduced arsenite-induced ER stress in N2a cells. In the parallel experiment, arsenite-induced disruption of intracellular calcium homeostasis was also ameliorated by taurine. The proven bio-function of taurine preserved a preventive effect against deleteriously cross-talking between oxidative stress, mitochondria, and ER. Overall, the results of the study suggested that taurine reinstated neuronal differentiation by inhibiting oxidative stress, ER stress, and mitochondrial dysfunction in arsenite-treated N2a cells.
Relation: 47(4), pp.735-744
URI: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/43577
Appears in Collections:[生命科學系] 期刊論文

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