Mitochondrial complex I deficiency in Parkinson's disease.

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.

journal_name

J Neurochem

authors

Schapira AH,Cooper JM,Dexter D,Clark JB,Jenner P,Marsden CD

doi

10.1111/j.1471-4159.1990.tb02325.x

subject

Has Abstract

pub_date

1990-03-01 00:00:00

pages

823-7

issue

3

eissn

0022-3042

issn

1471-4159

journal_volume

54

pub_type

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