Increased myocardial N-myristoyltransferase activity in rotenone model of Parkinsonism.
Identifieur interne : 001260 ( PubMed/Corpus ); précédent : 001259; suivant : 001261Increased myocardial N-myristoyltransferase activity in rotenone model of Parkinsonism.
Auteurs : Mohammed Khysar Pasha ; Rajendra K. Sharma ; Alexander H. RajputSource :
- International journal of molecular medicine [ 1107-3756 ] ; 2005.
English descriptors
- KwdEn :
- Acyl Coenzyme A (metabolism), Aminophylline (metabolism), Animals, Atropine (metabolism), Disease Models, Animal, Drug Combinations, Humans, Male, Nitroglycerin (metabolism), Papaverine (metabolism), Parkinson Disease (enzymology), Phenobarbital (metabolism), Rats, Rats, Inbred Lew, Rotenone (pharmacology).
- MESH :
- chemical , metabolism : Acyl Coenzyme A, Aminophylline, Atropine, Nitroglycerin, Papaverine, Phenobarbital.
- enzymology : Parkinson Disease.
- chemical , pharmacology : Rotenone.
- Animals, Disease Models, Animal, Drug Combinations, Humans, Male, Rats, Rats, Inbred Lew.
Abstract
There is widespread brain pathology in Parkinson's disease (PD), with the primary pathology in the substantia nigra. Oxidative stress is believed to play a role in cell death in PD. Rotenone is a mitochondrial toxin which can produce Parkinson syndrome (PS) in rats. Myristoyl-CoA:protein N-myristoyltransferase (NMT), which catalyzes the co-translational transfer of myristate from myristoyl-CoA to the amino-terminal glycine residue of selected polypeptides, is increased in the myocardium of ischemia-reperfusion rat model myocardium. Animals received rotoneone (n=10) or placebo vehicle (n=6) via Alzet osmotic pumps. Mean cardiac muscle NMT activity of placebo treated (control) rats was 0.608+/-0.366 units/mg protein. Rats with mild or no detectable PS features on rotenone showed slight (mean 0.853+/-0.192) but insignificantly increased activity. Rats that had moderately severe PS features had higher level of NMT activity (mean 1.223+/-0.057), which was borderline significant compared to controls (P=0.066). Rats with severe PS features had the highest NMT activity (1.353+/-0.128) which was significantly greater compared to controls (P=0.003) and to the rats that had equivocal or no motor slowing (P=0.005). Our data show cardiac metabolic dysfunction in a rotenone rat model of PS. The severity of this change correlates with the severity of motor manifestations. Further studies of NMT activity in human PD cases and patients with cardiomyopathy of unknown cause may provide valuable information in these disorders.
PubMed: 15870904
Links to Exploration step
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Rajput</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15870904</idno><idno type="pmid">15870904</idno><idno type="wicri:Area/PubMed/Corpus">001260</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001260</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Increased myocardial N-myristoyltransferase activity in rotenone model of Parkinsonism.</title><author><name sortKey="Pasha, Mohammed Khysar" sort="Pasha, Mohammed Khysar" uniqKey="Pasha M" first="Mohammed Khysar" last="Pasha">Mohammed Khysar Pasha</name><affiliation><nlm:affiliation>Division of Neurology, College of Medicine, Royal University Hospital, University of Saskatchewan, Saskatoon, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Sharma, Rajendra K" sort="Sharma, Rajendra K" uniqKey="Sharma R" first="Rajendra K" last="Sharma">Rajendra K. Sharma</name></author><author><name sortKey="Rajput, Alexander H" sort="Rajput, Alexander H" uniqKey="Rajput A" first="Alexander H" last="Rajput">Alexander H. Rajput</name></author></analytic><series><title level="j">International journal of molecular medicine</title><idno type="ISSN">1107-3756</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acyl Coenzyme A (metabolism)</term><term>Aminophylline (metabolism)</term><term>Animals</term><term>Atropine (metabolism)</term><term>Disease Models, Animal</term><term>Drug Combinations</term><term>Humans</term><term>Male</term><term>Nitroglycerin (metabolism)</term><term>Papaverine (metabolism)</term><term>Parkinson Disease (enzymology)</term><term>Phenobarbital (metabolism)</term><term>Rats</term><term>Rats, Inbred Lew</term><term>Rotenone (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Acyl Coenzyme A</term><term>Aminophylline</term><term>Atropine</term><term>Nitroglycerin</term><term>Papaverine</term><term>Phenobarbital</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Rotenone</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Drug Combinations</term><term>Humans</term><term>Male</term><term>Rats</term><term>Rats, Inbred Lew</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is widespread brain pathology in Parkinson's disease (PD), with the primary pathology in the substantia nigra. Oxidative stress is believed to play a role in cell death in PD. Rotenone is a mitochondrial toxin which can produce Parkinson syndrome (PS) in rats. Myristoyl-CoA:protein N-myristoyltransferase (NMT), which catalyzes the co-translational transfer of myristate from myristoyl-CoA to the amino-terminal glycine residue of selected polypeptides, is increased in the myocardium of ischemia-reperfusion rat model myocardium. Animals received rotoneone (n=10) or placebo vehicle (n=6) via Alzet osmotic pumps. Mean cardiac muscle NMT activity of placebo treated (control) rats was 0.608+/-0.366 units/mg protein. Rats with mild or no detectable PS features on rotenone showed slight (mean 0.853+/-0.192) but insignificantly increased activity. Rats that had moderately severe PS features had higher level of NMT activity (mean 1.223+/-0.057), which was borderline significant compared to controls (P=0.066). Rats with severe PS features had the highest NMT activity (1.353+/-0.128) which was significantly greater compared to controls (P=0.003) and to the rats that had equivocal or no motor slowing (P=0.005). Our data show cardiac metabolic dysfunction in a rotenone rat model of PS. The severity of this change correlates with the severity of motor manifestations. Further studies of NMT activity in human PD cases and patients with cardiomyopathy of unknown cause may provide valuable information in these disorders.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15870904</PMID><DateCreated><Year>2005</Year><Month>05</Month><Day>04</Day></DateCreated><DateCompleted><Year>2005</Year><Month>09</Month><Day>01</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1107-3756</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><Issue>6</Issue><PubDate><Year>2005</Year><Month>Jun</Month></PubDate></JournalIssue><Title>International journal of molecular medicine</Title><ISOAbbreviation>Int. J. Mol. Med.</ISOAbbreviation></Journal><ArticleTitle>Increased myocardial N-myristoyltransferase activity in rotenone model of Parkinsonism.</ArticleTitle><Pagination><MedlinePgn>987-91</MedlinePgn></Pagination><Abstract><AbstractText>There is widespread brain pathology in Parkinson's disease (PD), with the primary pathology in the substantia nigra. Oxidative stress is believed to play a role in cell death in PD. Rotenone is a mitochondrial toxin which can produce Parkinson syndrome (PS) in rats. Myristoyl-CoA:protein N-myristoyltransferase (NMT), which catalyzes the co-translational transfer of myristate from myristoyl-CoA to the amino-terminal glycine residue of selected polypeptides, is increased in the myocardium of ischemia-reperfusion rat model myocardium. Animals received rotoneone (n=10) or placebo vehicle (n=6) via Alzet osmotic pumps. Mean cardiac muscle NMT activity of placebo treated (control) rats was 0.608+/-0.366 units/mg protein. Rats with mild or no detectable PS features on rotenone showed slight (mean 0.853+/-0.192) but insignificantly increased activity. Rats that had moderately severe PS features had higher level of NMT activity (mean 1.223+/-0.057), which was borderline significant compared to controls (P=0.066). Rats with severe PS features had the highest NMT activity (1.353+/-0.128) which was significantly greater compared to controls (P=0.003) and to the rats that had equivocal or no motor slowing (P=0.005). Our data show cardiac metabolic dysfunction in a rotenone rat model of PS. The severity of this change correlates with the severity of motor manifestations. Further studies of NMT activity in human PD cases and patients with cardiomyopathy of unknown cause may provide valuable information in these disorders.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pasha</LastName><ForeName>Mohammed Khysar</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>Division of Neurology, College of Medicine, Royal University Hospital, University of Saskatchewan, Saskatoon, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharma</LastName><ForeName>Rajendra K</ForeName><Initials>RK</Initials></Author><Author ValidYN="Y"><LastName>Rajput</LastName><ForeName>Alexander H</ForeName><Initials>AH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. 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MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010634" MajorTopicYN="N">Phenobarbital</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011917" MajorTopicYN="N">Rats, Inbred Lew</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012402" MajorTopicYN="N">Rotenone</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>5</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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