The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Protective effect of the xanthate, D609, on Alzheimer's amyloid beta-peptide (1-42)-induced oxidative stress in primary neuronal cells.
Rukhsana Sultana; Shelley Newman; Hafiz Mohmmad-Abdul; Jeffery N Keller; D Allan Butterfield (Profiled Author: Butterfield, D Allan)
Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA.
Free radical research 2004;38(5):449-58.
Tricyclodecan-9-yl-xanthogenate (D609) is an inhibitor of phosphatidylcholine-specific phospholipase C, and this agent also has been reported to protect rodents against oxidative damage induced by ionizing radiation. Previously, we showed that D609 mimics glutathione (GSH) functions and that a disulfide is formed upon oxidation of D609 and the resulting dixanthate is a substrate for GSH reductase, regenerating D609. Considerable attention has been focused on increasing the intracellular GSH levels in many diseases, including Alzheimer's disease (AD). Amyloid beta-peptide [Abeta(1-42)], elevated in AD brain, is associated with oxidative stress and toxicity. The present study aimed to investigate the protective effects of D609 on Abeta(1-42)-induced oxidative cell toxicity in cultured neurons. Decreased cell survival in neuronal cultures treated with Abeta(1-42) correlated with increased free radical production measured by dichlorofluorescein fluorescence and an increase in protein oxidation (protein carbonyl, 3-nitrotyrosine) and lipid peroxidation (4-hydroxy-2-nonenal) formation. Pretreatment of primary hippocampal cultures with D609 significantly attenuated Abeta(1-42)-induced cytotoxicity, intracellular ROS accumulation, protein oxidation, lipid peroxidation and apoptosis. Methylated D609, with the thiol functionality no longer able to form the disulfide upon oxidation, did not protect neuronal cells against Abeta(1-42)-induced oxidative stress. Our results suggest that D609 exerts protective effects against Abeta(1-42) toxicity by modulating oxidative stress. These results may be of importance for the treatment of AD and other oxidative stress-related diseases.
1 Originating Grant
Markesbery, William R
15 May 1997 - 31 March 2013
NATIONAL INSTITUTE ON AGING
Total Funding: $ 17,393,197
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M Perluigi; G Joshi; R Sultana; V Calabrese; C De Marco; R Coccia; D A ButterfieldNeuroscience 2006;138(4):1161-70.
Hafiz Mohmmad Abdul; D Allan Butterfield
Protection against amyloid beta-peptide (1-42)-induced loss of phospholipid asymmetry in synaptosomal membranes by tricyclodecan-9-xanthogenate (D609) and ferulic acid ethyl ester: implications for Alzheimer's disease.Biochimica et biophysica acta 2005;1741(1-2):140-8.
Mubeen Ahmad Ansari; Gururaj Joshi; Quanzhen Huang; Wycliffe O Opii; Hafiz Mohmmad Abdul; Rukhsana Sultana; D Allan Butterfield
In vivo administration of D609 leads to protection of subsequently isolated gerbil brain mitochondria subjected to in vitro oxidative stress induced by amyloid beta-peptide and other oxidative stressors: relevance to Alzheimer's disease and other oxidative stress-related neurodegenerative disorders.Free radical biology & medicine 2006;41(11):1694-703.
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