Literature DB >> 20813403

The protective activities of water-soluble C(60) derivatives against nitric oxide-induced cytotoxicity in rat pheochromocytoma cells.

Zhen Hu1, Yudong Huang, Wenchao Guan, Jinglong Zhang, Feng Wang, Lei Zhao.   

Abstract

In this study, the protective activities of water-soluble C(60) derivatives against nitric oxide (NO) induced cytotoxicity were investigated. To overcome C(60) insolubility in water, we modified C(60) with β-alanine, valine or folacin. The compounds were characterized by FT-IR, (1)H NMR, (13)C NMR, LC-MS, elemental analysis, light scattering and TEM. Investigation of the possible NO-scavenging activities of water-soluble C(60) derivatives demonstrated that they expressed direct scavenging activity toward NO liberated within solution of sodium nitroprusside (SNP). In parallel, following exposure of cells to SNP (1 mM), a marked decrease in mitochondrial membrane potential, cell viability, activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), as well as increased levels of intracellular NO accumulation and malondialdehyde (MDA) production were observed. Moreover, SNP caused significant elevation in intracellular caspase-3 activity, and induced apoptotic death as determined by flow cytometric assay. However, pretreatment of the cells with water-soluble C(60) derivatives prior to SNP exposure blocked these NO-induced cellular events noticeably. Experiments demonstrated that the aggregation morphology could impact the NO-scavenging abilities and protective effects on apoptosis of water-soluble C(60) derivatives. The results suggest that water-soluble C(60) derivatives have the potential to prevent NO-mediated cell death without evident toxicity.
Copyright © 2010 Elsevier Ltd. All rights reserved.

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Year:  2010        PMID: 20813403     DOI: 10.1016/j.biomaterials.2010.08.025

Source DB:  PubMed          Journal:  Biomaterials        ISSN: 0142-9612            Impact factor:   12.479


  4 in total

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2.  Polyhydroxylated fullerene attenuates oxidative stress-induced apoptosis via a fortifying Nrf2-regulated cellular antioxidant defence system.

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Authors:  Lianjie Ye; Larwubah Kollie; Xing Liu; Wei Guo; Xiangxian Ying; Jun Zhu; Shengjie Yang; Meilan Yu
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  4 in total

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