Document Detail

Sulforaphane as an inducer of glutathione prevents oxidative stress-induced cell death in a dopaminergic-like neuroblastoma cell line.
MedLine Citation:
PMID:  19780897     Owner:  NLM     Status:  MEDLINE    
The total GSH depletion observed in the substantia nigra (SN) appears to be responsible for subsequent oxidative stress (OS), mitochondrial dysfunction, and dopaminergic cell loss in patients with Parkinson's disease. A strategy to prevent the OS of dopaminergic cells in the SN may be the use of chemopreventive agents as inducers of endogenous GSH, antioxidant and phase 2 enzymes. In this study, we demonstrated that treatment of the dopaminergic-like neuroblastoma SH-SY5Y cell line with sulforaphane (SF), a cruciferous vegetables inducer, resulted in significant increases of total GSH level, NAD(P)H : quinone oxidoreductase-1, GSH-transferase and -reductase, but not GSH-peroxidase, catalase and superoxide dismutase activities. Further, the elevation of GSH levels, GSH-transferase and NAD(P)H:quinone oxidoreductase-1 activities was correlated to an increase of the resistance of SH-SY5Y cells to toxicity induced by H(2)O(2) or 6-hydroxydopamine (6-OHDA). The pre-treatment of SH-SY5Y cells with SF was also shown to prevent various apoptotic events (mitochondrial depolarization, caspase 9 and 3 activation and DNA fragmentation) and necrosis elicited by 6-OHDA. Further, the impairment of antioxidant capacity and reactive oxygen species formation at intracellular level after exposure to 6-OHDA was effectively counteracted by pre-treatment with SF. Last, both the cytoprotective and antioxidant effects of SF were abolished by the addition of buthionine sulfoximine supporting the main role of GSH in the neuroprotective effects displayed by SF. These findings show that SF may play a role in preventing Parkinson's disease.
Andrea Tarozzi; Fabiana Morroni; Adriana Merlicco; Silvana Hrelia; Cristina Angeloni; Giorgio Cantelli-Forti; Patrizia Hrelia
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-09-22
Journal Detail:
Title:  Journal of neurochemistry     Volume:  111     ISSN:  1471-4159     ISO Abbreviation:  J. Neurochem.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-25     Completed Date:  2009-12-11     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  1161-71     Citation Subset:  IM    
Department of Pharmacology, Alma Mater Studiorum, University of Bologna, Bologna, Italy.
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MeSH Terms
Adrenergic Agents / pharmacology
Analysis of Variance
Anticarcinogenic Agents / pharmacology*
Caspase 3 / metabolism
Caspase 9 / metabolism
Cell Death / drug effects
Cell Line, Tumor
DNA Fragmentation / drug effects
Dopamine / metabolism*
Dose-Response Relationship, Drug
Drug Interactions
Enzyme-Linked Immunosorbent Assay / methods
Glutathione / metabolism*
Hydrogen Peroxide / pharmacology
Membrane Potential, Mitochondrial / drug effects,  physiology
Neuroblastoma / pathology
Oxidative Stress / drug effects*,  physiology*
Oxidopamine / pharmacology
Thiocyanates / pharmacology*
Time Factors
Reg. No./Substance:
0/Adrenergic Agents; 0/Anticarcinogenic Agents; 0/Thiocyanates; 1199-18-4/Oxidopamine; 4478-93-7/sulforafan; 70-18-8/Glutathione; 7722-84-1/Hydrogen Peroxide; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 9

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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