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Titolo:
QUANTITATIVE STUDY OF MITOCHONDRIAL COMPLEX-I IN PLATELETS OF PARKINSONIAN-PATIENTS
Autore:
BLANDINI F; NAPPI G; GREENAMYRE JT;
Indirizzi:
UNIV PAVIA,NEUROL INST C MONDINO,LAB FUNCT NEUROCHEM,VIA PALESTRO 3 I-27100 PAVIA ITALY EMORY UNIV,DEPT NEUROL ATLANTA GA 30322
Titolo Testata:
Movement disorders
fascicolo: 1, volume: 13, anno: 1998,
pagine: 11 - 15
SICI:
0885-3185(1998)13:1<11:QSOMCI>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
H-3 DIHYDROROTENONE BINDING; ELECTRON-TRANSPORT CHAIN; RESPIRATORY-CHAIN; SKELETAL-MUSCLE; 1-METHYL-4-PHENYLPYRIDINIUM ION; NADH DEHYDROGENASE; SUBSTANTIA-NIGRA; DISEASE; BRAIN; NEUROTOXIN;
Keywords:
PLATELET; ENERGY METABOLISM; [H-3]DIHYDROROTENONE; MITOCHONDRIA; COMPLEX I; 1-METHYL-4-PHENYL-PYRIDINIUM (MPP+); PARKINSONS DISEASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
F. Blandini et al., "QUANTITATIVE STUDY OF MITOCHONDRIAL COMPLEX-I IN PLATELETS OF PARKINSONIAN-PATIENTS", Movement disorders, 13(1), 1998, pp. 11-15

Abstract

Activity of mitochondrial enzyme complex I (NADH-ubiquinone oxidoreductase) is reduced in the substantia nigra of patients with Parkinson'sdisease (PD). A less pronounced decrease in the activity of this enzyme has also been reported in platelets of PD patients. To obtain quantitative information on platelet complex I in PD, we studied platelet complex I in 16 PD patients and 16 age-matched controls by using a newly developed technique based on the binding of [H-3]dihydrorotenone ([H-3]DHR), an analog of the pesticide rotenone, to complex I. We also investigated the inhibitory effect of MPP+ (1-methyl-4-phenyl-pyridinium) on [H-3]DHR specific binding to platelet complex I. PD patients and controls showed similar levels of [H-3]DHR specific binding; preincubation of platelets with MPP+ caused the same degree of inhibition of [3H]DHR specific binding in the two groups. In PD patients, we observed a direct correlation between MPP+-induced inhibition of [H-3]DHR specific binding and the daily intake of levodopa, which may be related to drug-induced changes in the transport of MPP+ into the platelet or in its binding to complex I. These findings demonstrate that the reportedreduction in complex I activity in platelets of PD patients can not be accounted for by an abnormality at the level of the rotenone bindingsite (putatively the ND-1 gene product), although they do not excludedifferences in complex I activity between PD patients and controls.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 21:30:11