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Molecules 2016, 21(6), 637; doi:10.3390/molecules21060637

ESeroS-GS Protects Neuronal Cells from Oxidative Stress by Stabilizing Lysosomes

1
National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China
2
University of Chinese Academy of Sciences, Beijing 100049, China
*
Author to whom correspondence should be addressed.
Academic Editor: Maurizio Battino
Received: 24 March 2016 / Revised: 9 May 2016 / Accepted: 10 May 2016 / Published: 25 May 2016
(This article belongs to the Section Medicinal Chemistry)
View Full-Text   |   Download PDF [3373 KB, uploaded 25 May 2016]   |  

Abstract

γ-l-glutamyl-S-[2-[[[3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H-1-benzopyran-6-yl]oxy]carbonyl]-3-[[2-(1H-indol-3-yl)ethyl]amino]-3-oxopropyl]-l-cysteinylglycine sodium salt (ESeroS-GS) is a water-soluble derivative of α-tocopherol (vitamin E). We reported previously that ESeroS-GS can act as an anti-inflammatory agent and can induce cell death in breast cancer cells. However, the potential antioxidant capacities of ESeroS-GS remain elusive. Here, we measured its scavenging effects on free radicals and evaluated its protective effects on neuronal cells against oxidative stress. The results indicated that ESeroS-GS effectively scavenged both 2,2’-azinobis(3-ethylbenzothiazoline)-6-sulfonate free radicals (ABTS•+) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radicals, and attenuated H2O2-induced neuronal cell death. H2O2 treatment induced lysosomal membrane permeabilization rapidly, and caused the redistribution of lysosomal proteases, which were responsible for the neuronal cell death. ESeroS-GS abolished the interaction between tBid and the lysosomal membranes, blocked the translocation of tBid to the lysosomal membranes, decreased its oligomerization within the membrane circumstances, prevented the lysosomal membrane permeabilization, and thus attenuated the neuronal cell death. These data suggest that ESeroS-GS protected the neuronal cells from oxidative stress by stabilizing lysosomal membranes, and thus might act as a novel neuroprotector for neuronal diseases associated with oxidative stress. View Full-Text
Keywords: ESeroS-GS; antioxidant; neuronal cell; cell death; oxidative stress; lysosome; Bid ESeroS-GS; antioxidant; neuronal cell; cell death; oxidative stress; lysosome; Bid
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Yang, N.; Chen, Q.; He, X.; Zhao, X.; Wei, T. ESeroS-GS Protects Neuronal Cells from Oxidative Stress by Stabilizing Lysosomes. Molecules 2016, 21, 637.

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