Taurine resumed neuronal differentiation in arsenite-treated N2a cells through reducing oxidative stress,endoplasmic reticulum stress,and mitochondrial dysfunction |
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Authors: | Chien-Te?Chou,Hong-Ting?Lin,Pai-An?Hwang,Shang-Ta?Wang,Cheng-Hong?Hsieh,Deng-Fwu?Hwang author-information" > author-information__contact u-icon-before" > mailto:dfhwang@mail.ntou.edu.tw" title=" dfhwang@mail.ntou.edu.tw" itemprop=" email" data-track=" click" data-track-action=" Email author" data-track-label=" " >Email author |
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Affiliation: | 1.Department of Food Science,National Taiwan Ocean University,Keelung,Taiwan, ROC;2.Department of Agricultural Chemistry,National Taiwan University,Taipei,Taiwan, ROC;3.Department of Health and Nutrition Biotechnology,Asia University,Taichung,Taiwan, ROC;4.Seafood Technology Division, Fisheries Research Institute,Council of Agriculture,Keelung,Taiwan, ROC |
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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. |
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