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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2012) 36, 677–681 (Printed in Great Britain)
Protection of cells from nitric oxide-mediated apoptotic death by glutathione C60 derivative
Zhen Hu, Chunhua Zhang1, Peiyi Tang, Cuiyun Li, Yuhuan Yao, Shaofan Sun, Li Zhang and Yudong Huang1
School of Chemical Engineering and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin 150001, Peoples Republic of China


The influence of the glutathione C60 derivative on the cytotoxicity of a highly reactive free radical NO (nitric oxide) has been investigated. Consistent with its cytoprotective abilities, the derivative scavenges ROS (reactive oxygen species) and RNS (reactive nitrogen species) both in vitro and under cell-free conditions. Moreover, the glutathione C60 derivative protected PC12 cells from the cytotoxic effect of the NO-releasing compound, SNP (sodium nitroprusside). Addition of glutathione C60 derivative alone did not induce apoptosis and necrosis. The results suggest that the glutathione C60 derivative has the potential to prevent NO-mediated cell death without evident toxicity.


Key words: antioxidant, apoptosis, cytotoxicity, fullerene, nitric oxide

Abbreviations: DAF, diaminofluorescein, DHR, dihydrorhodamine, DMEM, Dulbecco's modified Eagle's medium, MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide, NO, nitric oxide, OGFD, oxidized glutathione C60 derivative, PI, propidium iodide, RNS, reactive nitrogen species, ROS, reactive oxygen species, SNP, sodium nitroprusside

1Correspondence may be addressed to either of these authors (email yudong.huang@yahoo.com.cn or zhangchunhua@hit.edu.cn).


Received 23 October 2011/18 January 2012; accepted 22 March 2012

Published as Cell Biology International Immediate Publication 22 March 2012, doi:10.1042/CBI20110566


© The Author(s) Journal compilation © 2012 International Federation for Cell Biology


ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)