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NGF attenuates 3-nitrotyrosine formation in a 3-NP model of Huntington's disease

dc.contributor.authorGalpern, Wendy R.
dc.contributor.authorMatthews, Russell T.
dc.contributor.authorBeal, M. Flint
dc.contributor.authorIsacson, Ole
dc.date2022-08-11T08:08:57.000
dc.date.accessioned2022-08-23T16:13:47Z
dc.date.available2022-08-23T16:13:47Z
dc.date.issued1996-11-04
dc.date.submitted2008-09-10
dc.identifier.citationNeuroreport. 1996 Nov 4;7(15-17):2639-42.
dc.identifier.issn0959-4965 (Print)
dc.identifier.pmid8981438
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33705
dc.description.abstractNerve growth factor (NGF)-secreting fibroblasts are able to protect against the Huntington-like striatal neurodegeneration induced by the mitochondrial toxin 3-nitropropionic acid (3-NP). In the present study, we investigated whether the neuroprotective effects of NGF are mediated through antioxidative mechanisms. Rats were grafted in the corpus callosum with NGF[+] or NGF[-] fibroblasts 7 days before administration of 3-NP. The generation of peroxynitrite was evaluated by measuring the striatal levels of 3-nitrotyrosine. NGF significantly decreased the 3-NP induced generation of 3-nitrotyrosine, presumably by decreasing peroxynitrite formation. These findings suggest that NGF might protect against neuronal death by inhibiting the production of nitric oxide or decreasing the levels of superoxide radicals, thereby decreasing the generation of oxidative agents such as peroxynitrite.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8981438&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://bs7xv3ec2w.search.serialssolutions.com/?sid=Entrez:PubMed&id=pmid:8981438
dc.subjectAnimals; Corpus Striatum; Disease Models, Animal; Huntington Disease; Male; Nerve Growth Factors; Nitro Compounds; Propionic Acids; Rats; Rats, Sprague-Dawley; Tyrosine
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleNGF attenuates 3-nitrotyrosine formation in a 3-NP model of Huntington's disease
dc.typeJournal Article
dc.source.journaltitleNeuroreport
dc.source.volume7
dc.source.issue15-17
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/369
dc.identifier.contextkey625996
html.description.abstract<p>Nerve growth factor (NGF)-secreting fibroblasts are able to protect against the Huntington-like striatal neurodegeneration induced by the mitochondrial toxin 3-nitropropionic acid (3-NP). In the present study, we investigated whether the neuroprotective effects of NGF are mediated through antioxidative mechanisms. Rats were grafted in the corpus callosum with NGF[+] or NGF[-] fibroblasts 7 days before administration of 3-NP. The generation of peroxynitrite was evaluated by measuring the striatal levels of 3-nitrotyrosine. NGF significantly decreased the 3-NP induced generation of 3-nitrotyrosine, presumably by decreasing peroxynitrite formation. These findings suggest that NGF might protect against neuronal death by inhibiting the production of nitric oxide or decreasing the levels of superoxide radicals, thereby decreasing the generation of oxidative agents such as peroxynitrite.</p>
dc.identifier.submissionpathgsbs_sp/369
dc.contributor.departmentNeuroregeneration Laboratory
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages2639-42


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