Green tea polyphenols enhance sodium nitroprusside-induced neurotoxicity in human neuroblastoma SH-SY5Y cells
Autor: | Yue-ting Zhang, Baolu Zhao |
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Rok vydání: | 2003 |
Předmět: |
chemistry.chemical_classification
Reactive oxygen species SH-SY5Y Chemistry Neurotoxicity food and beverages Glutathione medicine.disease_cause medicine.disease Biochemistry Nitric oxide Cellular and Molecular Neuroscience chemistry.chemical_compound medicine Viability assay Sodium nitroprusside Oxidative stress medicine.drug |
Zdroj: | Journal of Neurochemistry. 86:1189-1200 |
ISSN: | 1471-4159 0022-3042 |
DOI: | 10.1046/j.1471-4159.2003.01928.x |
Popis: | Oxidative stress is a main mediator in nitric oxide (NO) -induced neurotoxicity and has been implicated in the pathogenesis of many neurodegenerative disorders. Green tea polyphenols are usually expected as potent chemo-preventive agents due to their ability of scavenging free radicals and chelating metal ions. However, not all the actions of green tea polyphenols are necessarily beneficial. In the present study, we demonstrated that higher-concentration green tea ployphenols significantly enhanced the neurotoxicity by treatment of sodium nitroprusside (SNP), a nitric oxide donor. SNP induced apoptosis in human neuroblastoma SH-SY5Y cells in a concentration and time-dependent manner, as estimated by cell viability assessment, FACScan analysis and DNA fragmentation assay, whereas treatment with green tea polyphenols alone had no effect on cell viability. Pre-treatment with lower-dose green tea polyphenols (50 and 100 lM) had only a slightly deleterious effect in the presence of SNP, while higher-dose green tea polyphenols (200 and 500 lM) synergistically damaged the cells severely. Further research showed that co-incubation of green tea polyphenols and SNP caused loss of mitochondrial membrane potential, depletion of intracellular GSH and accumulation of reactive oxygen species, and exacerbated NO-induced neuronal apoptosis via a Bcl-2 sensitive pathway. |
Databáze: | OpenAIRE |
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