| Astaxanthin protects against MPTP/MPP+-induced mitochondrial dysfunction and ROS production in vivo and in vitro. | |
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MedLine Citation:
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PMID: 21056612 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Astaxanthin (AST) is a powerful antioxidant that occurs naturally in a wide variety of living organisms. We have investigated the role of AST in preventing 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced apoptosis of the substantia nigra (SN) neurons in the mouse model of Parkinson's disease (PD) and 1-methyl-4-phenylpyridinium (MPP+)-induced cytotoxicity of SH-SY5Y human neuroblastoma cells. In in vitro study, AST inhibits MPP+-induced production of intracellular reactive oxygen species (ROS) and cytotoxicity in SH-SY5Y human neuroblastoma cells. Preincubation of AST (50 μM) significantly attenuates MPP+-induced oxidative damage. Furthermore, AST is able to enhance the expression of Bcl-2 protein but reduce the expression of α-synuclein and Bax, and suppress the cleavage of caspase-3. Our results suggest that the protective effects of AST on MPP+-induced apoptosis may be due to its anti-oxidative properties and anti-apoptotic activity via induction of expression of superoxide dismutase (SOD) and catalase and regulating the expression of Bcl-2 and Bax. Pretreatment with AST (30 mg/kg) markedly increases tyrosine hydroxylase (TH)-positive neurons and decreases the argyrophilic neurons compared with the MPTP model group. In summary, AST shows protection from MPP+/MPTP-induced apoptosis in the SH-SY5Y cells and PD model mouse SN neurons, and this effect may be attributable to upregulation of the expression of Bcl-2 protein, downregulation of the expression of Bax and α-synuclein, and inhibition of the activation of caspase-3. These data indicate that AST may provide a valuable therapeutic strategy for the treatment of progressive neurodegenerative disease such as Parkinson's disease. |
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Authors:
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Dae-Hee Lee; Cuk-Seong Kim; Yong J Lee |
Publication Detail:
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Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-11-05 |
Journal Detail:
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Title: Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Volume: 49 ISSN: 1873-6351 ISO Abbreviation: Food Chem. Toxicol. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-24 Completed Date: 2011-05-05 Revised Date: 2012-01-04 |
Medline Journal Info:
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Nlm Unique ID: 8207483 Medline TA: Food Chem Toxicol Country: England |
Other Details:
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Languages: eng Pagination: 271-80 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Surgery, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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1-Methyl-4-phenylpyridinium
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toxicity* Animals Antioxidants / pharmacology* Caspase 3 / metabolism Catalase / biosynthesis Cell Line, Tumor Cytochromes / metabolism Enzyme Activation Enzyme Induction Fluorescent Antibody Technique, Indirect Humans MPTP Poisoning / metabolism, physiopathology, prevention & control* Mice Mice, Inbred BALB C Mitochondria / drug effects*, metabolism, physiology Oxidative Stress Reactive Oxygen Species / metabolism* Superoxide Dismutase / biosynthesis Xanthophylls / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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CA140554/CA/NCI NIH HHS; R01 CA140554-02/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/Cytochromes; 0/Reactive Oxygen Species; 0/Xanthophylls; 472-61-7/astaxanthine; 48134-75-4/1-Methyl-4-phenylpyridinium; EC 1.11.1.6/Catalase; EC 1.15.1.1/Superoxide Dismutase; EC 3.4.22.-/Caspase 3 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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