MITOCHONDRIAL COMPLEX I DEFICIENCY IN PARKINSONS-DISEASE

被引：1724

作者：

SCHAPIRA, AHV

COOPER, JM

DEXTER, D

CLARK, JB

JENNER, P

MARSDEN, CD

机构：

[1] UNIV LONDON KINGS COLL HOSP,SCH MED,DEPT BIOCHEM,LONDON SE5 8RX,ENGLAND

[2] UNIV LONDON,INST NEUROL,DEPT CLIN NEUROL,LONDON,ENGLAND

[3] ST BARTHOLOMEWS HOSP & MED COLL,DEPT BIOCHEM,LONDON EC1A 7BE,ENGLAND

[4] UNIV LONDON KINGS COLL HOSP,SCH MED,LONDON SE5 8RX,ENGLAND

[5] UNIV LONDON,INST PSYCHIAT,DEPT NEUROL,PARKINSONS DIS SOC RES CTR,LONDON,ENGLAND

来源：

JOURNAL OF NEUROCHEMISTRY | 1990年 / 54卷 / 03期

关键词：

1‐Methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine; Complex I; Mitochondria; Parkinson's disease;

D O I：

10.1111/j.1471-4159.1990.tb02325.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Abstract: The structure and function of mitochondrial respiratory‐chain enzyme proteins were studied postmortem in the substantia nigra of nine patients with Parkinson's disease and nine matched controls. Total protein and mitochondrial mass were similar in the two groups. NADH‐ubiquinone reductase (Complex I) and NADH cytochrome c reductase activities were significantly reduced, whereas succinate cytochrome c reductase activity was normal. These results indicated a specific defect of Complex I activity in the substantia nigra of patients with Parkinson's disease. This biochemical defect is the same as that produced in animal models of parkinsonism by 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) and adds further support to the proposition that Parkinson's disease may be due to an environmental toxin with action(s) similar to those of MPTP. Copyright © 1990, Wiley Blackwell. All rights reserved

引用

页码：823 / 827

页数：5

共 37 条

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