Platelet mitochondrial respiratory chain function in Parkinson's disease
β Scribed by C. I. Blake; E. Spitz; M. Leehey; Dr. B. J. Hoffer; S. J. Boyson
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 644 KB
- Volume
- 12
- Category
- Article
- ISSN
- 0885-3185
No coin nor oath required. For personal study only.
β¦ Synopsis
Abstract
Reports on mitochondrial respiratory chain (MRC) complex I (CI) dysfunction in the substantia nigra in Parkinson's disease (PD) support the oxidative stress hypothesis in the neuropathogenesis of PD. Studies in peripheral tissue have found variable decreased CI and occasionally other complex activity suggestive of systemic impairment of MRC function in PD; however, MRC activity may be influenced by numerous variables. We conducted spectrophotometric measurements of MRC function in platelet mitochondrial preparations in 13 individuals with PD and 9 ageβmatched controls (CON) and have identified additional variables that may affect MRC activity. Mean CI, CIII, CIV, and citrate synthase (CS) activities were similar between PD and CON. CIII and CIV, specific and CSβcorrected, activities were significantly positively correlated with CI in combined and individual group data, with the exception of CIII CSβcorrected and CIV specific activities in CON and PD, respectively. CIII and CS specific activities were negatively correlated with age in CON, but varied randomly in PD. In PD, CIII specific activity was 1.4βfold higher in those with a history of environmental risk factors for PD and CIV specific activity was lower in those with a positive family history of PD [8.34 Β± 0.74 (n = 4) vs. 12.4 Β± 1.1 (SEM) min^β1^ mg^β1^; p = 0.046]. Group heterogeneity, variables affecting enzyme activity, and intrinsic properties of cells may thus contribute to conflicting data in studies of MRC function in platelets and other tissues.
π SIMILAR VOLUMES
## Abstract Oxygen consumption and enzyme activity were evaluted in platelet mitochondria from 17 patients with Parkinson's disease. In comparison with ageβmatched controls, no consistent abnormality could be discerned in complex I, complex IIβIII, or complex IV oxygen consumption, or in the enzyme
## Abstract Multiple system atrophy (MSA) is a clinicopathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5β10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activit