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dc.contributor.authorTorsdottir, G
dc.contributor.authorKristinsson, J
dc.contributor.authorSveinbjornsdottir, S
dc.contributor.authorSnaedal, J
dc.contributor.authorJohannesson, T
dc.date.accessioned2010-07-29T11:16:47Z
dc.date.available2010-07-29T11:16:47Z
dc.date.issued1999-11-01
dc.date.submitted2010-07-10
dc.identifier.citationPharmacol. Toxicol. 1999, 85(5):239-43en
dc.identifier.issn0901-9928
dc.identifier.pmid10608487
dc.identifier.doi10.1111/j.1600-0773.1999.tb02015.x
dc.identifier.urihttp://hdl.handle.net/2336/108617
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractIn a previous study we found copper dyshomeostasis in patients with Alzheimer's disease. In this study, levels of copper in plasma, of ceruloplasmin in serum and ceruloplasmin oxidative activity as well as superoxide dismutase (SOD) activity in erythrocytes were determined in 40 patients with Parkinson's disease and their healthy age- and gender-matched controls. Copper concentrations did not differ significantly in the two groups, whereas both ceruloplasmin concentrations and ceruloplasmin oxidative activity were significantly lower in the patients, also relative to ceruloplasmin mass. SOD activity was not significantly different in the two groups but decreased significantly with the duration of disease. The same was found for ceruloplasmin oxidative activity. Ceruloplasmin oxidative activity and SOD activity did not decrease with age. Levels of serum iron, serum ferritin and total iron binding capacity were determined in about 30 of the patients and an equal number of controls and were not found to differ. Transferrin levels were significantly lower in the patients than in their controls but, conversely, the transferrin saturation was significantly higher in the patients. The results indicate that patients with Alzheimer's disease and Parkinson's disease have defective ceruloplasmin and SOD activities in common and that these defects are not necessarily associated with major disturbances in iron homeostasis.
dc.language.isoenen
dc.relation.urlhttp://dx.doi.org/10.1111/j.1600-0773.1999.tb02015.xen
dc.subject.meshAge Factorsen
dc.subject.meshAgeden
dc.subject.meshCeruloplasminen
dc.subject.meshCopperen
dc.subject.meshFemaleen
dc.subject.meshFerritinsen
dc.subject.meshHumansen
dc.subject.meshIronen
dc.subject.meshMaleen
dc.subject.meshMiddle Ageden
dc.subject.meshParkinson Diseaseen
dc.subject.meshSuperoxide Dismutaseen
dc.subject.meshTime Factorsen
dc.titleCopper, ceruloplasmin, superoxide dismutase and iron parameters in Parkinson's disease.en
dc.typeArticleen
dc.contributor.departmentDepartment of Pharmacology and Toxicology, The Institute of Pharmacy, Pharmacology and Toxicology, University of Iceland.en
dc.identifier.journalPharmacology & toxicologyen
html.description.abstractIn a previous study we found copper dyshomeostasis in patients with Alzheimer's disease. In this study, levels of copper in plasma, of ceruloplasmin in serum and ceruloplasmin oxidative activity as well as superoxide dismutase (SOD) activity in erythrocytes were determined in 40 patients with Parkinson's disease and their healthy age- and gender-matched controls. Copper concentrations did not differ significantly in the two groups, whereas both ceruloplasmin concentrations and ceruloplasmin oxidative activity were significantly lower in the patients, also relative to ceruloplasmin mass. SOD activity was not significantly different in the two groups but decreased significantly with the duration of disease. The same was found for ceruloplasmin oxidative activity. Ceruloplasmin oxidative activity and SOD activity did not decrease with age. Levels of serum iron, serum ferritin and total iron binding capacity were determined in about 30 of the patients and an equal number of controls and were not found to differ. Transferrin levels were significantly lower in the patients than in their controls but, conversely, the transferrin saturation was significantly higher in the patients. The results indicate that patients with Alzheimer's disease and Parkinson's disease have defective ceruloplasmin and SOD activities in common and that these defects are not necessarily associated with major disturbances in iron homeostasis.


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