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dc.contributor.authorHenninger, Nils
dc.contributor.authorWang, Qi
dc.contributor.authorOkun, Jurgen G.
dc.contributor.authorSchwab, Stefan
dc.contributor.authorKrause, Martin
dc.date2022-08-11T08:09:28.000
dc.date.accessioned2022-08-23T16:31:56Z
dc.date.available2022-08-23T16:31:56Z
dc.date.issued2007-12-01
dc.date.submitted2016-05-10
dc.identifier.citationParkinsonism Relat Disord. 2007 Dec;13(8):524-7. Epub 2007 Jan 19. <a href="http://dx.doi.org/10.1016/j.parkreldis.2006.11.005">Link to article on publisher's site</a>
dc.identifier.issn1353-8020 (Linking)
dc.identifier.doi10.1016/j.parkreldis.2006.11.005
dc.identifier.pmid17240187
dc.identifier.urihttp://hdl.handle.net/20.500.14038/37768
dc.description.abstractBACKGROUND: This study investigated whether brief exposure to nitrous oxide (N(2)O) exacerbates levodopa-induced hyperhomocysteinemia, and if co-treatment with folate or entacapone could reduce total plasma homocysteine (tHcy) levels. METHODS: Male Wistar rats (N=9 per group) were randomly treated with vehicle/N(2)O (GROUP 1), levodopa/nitrogen (group 2), levodopa/N(2)O (group 3), levodopa/N(2)O+folate (group 4), or levodopa/N(2)O+entacapone (group 5). tHcy was measured at 12 min, 4, 8, and 12 h after anesthesia. RESULTS AND CONCLUSION: The combination of N(2)O-exposure and levodopa treatment significantly increased tHcy in rats. This hyperhomocysteinemia could be prevented by entacapone but not folate co-administration.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17240187&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.parkreldis.2006.11.005
dc.subjectAnalgesics, Non-Narcotic
dc.subjectAnalysis of Variance
dc.subjectAnimals
dc.subjectCatechols
dc.subjectDrug Interactions
dc.subjectEnzyme Inhibitors
dc.subjectHomocysteine
dc.subjectHyperhomocysteinemia
dc.subjectImmunoassay
dc.subject*Levodopa
dc.subjectMale
dc.subjectNitriles
dc.subjectNitrous Oxide
dc.subjectRandom Allocation
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectNervous System Diseases
dc.subjectNeurology
dc.subjectNeuroscience and Neurobiology
dc.titleNitrous oxide promotes hyperhomocysteinemia in levodopa treated rats
dc.typeJournal Article
dc.source.journaltitleParkinsonism and related disorders
dc.source.volume13
dc.source.issue8
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neuro_pp/449
dc.identifier.contextkey8585908
html.description.abstract<p>BACKGROUND: This study investigated whether brief exposure to nitrous oxide (N(2)O) exacerbates levodopa-induced hyperhomocysteinemia, and if co-treatment with folate or entacapone could reduce total plasma homocysteine (tHcy) levels.</p> <p>METHODS: Male Wistar rats (N=9 per group) were randomly treated with vehicle/N(2)O (GROUP 1), levodopa/nitrogen (group 2), levodopa/N(2)O (group 3), levodopa/N(2)O+folate (group 4), or levodopa/N(2)O+entacapone (group 5). tHcy was measured at 12 min, 4, 8, and 12 h after anesthesia.</p> <p>RESULTS AND CONCLUSION: The combination of N(2)O-exposure and levodopa treatment significantly increased tHcy in rats. This hyperhomocysteinemia could be prevented by entacapone but not folate co-administration.</p>
dc.identifier.submissionpathneuro_pp/449
dc.contributor.departmentDepartment of Neurology
dc.source.pages524-7


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