Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations
Identifieur interne : 001577 ( Istex/Corpus ); précédent : 001576; suivant : 001578Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations
Auteurs : Meltem Müftüoglu ; Bülent Elibol ; Özlem Dalm Zrak ; Ayse Ercan ; Gülnihal Kulaks Z ; Hamdi Ögüs ; Turgay Dalkara ; Nazmi ÖzerSource :
- Movement Disorders [ 0885-3185 ] ; 2004-05.
English descriptors
- KwdEn :
Abstract
The parkin protein functions as a RING‐type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin‐proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age‐matched controls (P < 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. © 2003 Movement Disorder Society
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DOI: 10.1002/mds.10695
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<creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Turgay</givenNames>
<familyName>Dalkara</familyName>
<degrees>MD, PhD</degrees>
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<creator xml:id="au8" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Nazmi</givenNames>
<familyName>Özer</familyName>
<degrees>PhD</degrees>
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<contactDetails><email>naozer@hacettepe.edu.tr</email>
</contactDetails>
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<affiliationGroup><affiliation xml:id="af1" countryCode="TR" type="organization"><unparsedAffiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</unparsedAffiliation>
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<affiliation xml:id="af2" countryCode="TR" type="organization"><unparsedAffiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</unparsedAffiliation>
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<keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword>
<keyword xml:id="kwd2">complex I</keyword>
<keyword xml:id="kwd3">complex IV</keyword>
<keyword xml:id="kwd4">mtDNA</keyword>
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<fundingInfo><fundingAgency>Scientific and Technical Research Council of Turkey</fundingAgency>
<fundingNumber>SBAG‐2596</fundingNumber>
<fundingNumber>TBAG‐1754</fundingNumber>
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<fundingInfo><fundingAgency>Hacettepe University Scientific Research Unit</fundingAgency>
<fundingNumber>0002101001</fundingNumber>
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<p>The parkin protein functions as a RING‐type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin‐proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age‐matched controls (<i>P</i>
< 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. © 2003 Movement Disorder Society</p>
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<!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title>
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<titleInfo type="abbreviated" lang="en"><title>Mitochondrial Enyzmes in Parkinson's Disease</title>
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<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations</title>
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<name type="personal"><namePart type="given">Meltem</namePart>
<namePart type="family">Müftüoglu</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation>
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</name>
<name type="personal"><namePart type="given">Bülent</namePart>
<namePart type="family">Elibol</namePart>
<namePart type="termsOfAddress">MD, PhD</namePart>
<affiliation>Department of Neurology, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation>
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</name>
<name type="personal"><namePart type="given">Özlem</namePart>
<namePart type="family">Dalmızrak</namePart>
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<affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation>
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</role>
</name>
<name type="personal"><namePart type="given">Ayse</namePart>
<namePart type="family">Ercan</namePart>
<namePart type="termsOfAddress">MSc</namePart>
<affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Gülnihal</namePart>
<namePart type="family">Kulaksız</namePart>
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<name type="personal"><namePart type="given">Hamdi</namePart>
<namePart type="family">Ögüs</namePart>
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<affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation>
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</name>
<name type="personal"><namePart type="given">Turgay</namePart>
<namePart type="family">Dalkara</namePart>
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<name type="personal"><namePart type="given">Nazmi</namePart>
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<affiliation>Department of Biochemistry, Hacettepe University, Faculty of Medicine, Ankara, Turkey</affiliation>
<description>Correspondence: Hacettepe University, Faculty of Medicine, Department of Biochemistry, 06100, Sıhhiye, Ankara, Turkey</description>
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<dateCaptured encoding="w3cdtf">2003-06-05</dateCaptured>
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<abstract lang="en">The parkin protein functions as a RING‐type ubiquitin protein ligase. Considering the possibility that impaired ubiquitin‐proteosomal system activity may impair antioxidant defenses and enhance oxidative stress, we have investigated the activity of mitochondrial respiratory enzymes in patients with parkin gene mutations. A significant decrease in the leukocyte complex I activity was found both in patients with parkin mutations (62.5%) and idiopathic PD (64.5%) compared with age‐matched controls (P < 0.001). Complex IV activity was also decreased significantly in idiopathic PD patients (60%), but no difference was detected between controls and patients with parkin mutations. © 2003 Movement Disorder Society</abstract>
<note type="funding">Scientific and Technical Research Council of Turkey - No. SBAG‐2596; No. TBAG‐1754; </note>
<note type="funding">Hacettepe University Scientific Research Unit - No. 0002101001; </note>
<subject lang="en"><genre>Keywords</genre>
<topic>Parkinson's disease</topic>
<topic>complex I</topic>
<topic>complex IV</topic>
<topic>mtDNA</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
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<titleInfo type="abbreviated"><title>Mov. Disord.</title>
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<topic>Brief Report</topic>
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<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part><date>2004</date>
<detail type="volume"><caption>vol.</caption>
<number>19</number>
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<detail type="issue"><caption>no.</caption>
<number>5</number>
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<extent unit="pages"><start>544</start>
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