home >
articles >
parkinson's disease > Altered mitochondrial function, iron metabolism
and glutathione levels in Parkinson's disease
Glutathione Articles - Parkinson's Disease
Altered mitochondrial function, iron metabolism and glutathione levels
in Parkinson's disease
Jenner P.
Parkinson's Disease Society, King's College London, UK.
Acta Neurol Scand Suppl. 1993;146:6-13.Links
ABSTRACT
The mechanisms underlying dopamine cell death in substantia nigra in
Parkinson's disease remain unknown. Current concepts of this process suggest
the involvement of free radical species and oxidative stress. Indeed, in
postmortem tissues from patients dying with Parkinson's disease there is
evidence for inhibition of complex I of the mitochondrial respiratory chain,
altered iron metabolism and decreased levels of reduced glutathione.
However, alterations in iron levels in substantia nigra are not specific to
Parkinson's disease but also occur in other basal ganglia degenerative
diseases. So, alterations in iron may be a response to, rather than a cause
of nigral cell death. This is further suggested by a failure to find any
alterations in iron metabolism in cases of incidental Lewy body disease (presymptomatic
Parkinson's disease). Similarly, in these tissues no significant alteration
in complex I activity is apparent. However, there is a reduction in the
levels of reduced glutathione in substantia nigra in incidental Lewy body
disease of the same magnitude as occurs in advanced Parkinson's disease.
This would suggest that alterations in glutathione function are an early
marker of pathology in Parkinson's disease and may be a clue to the primary
cause of nigral cell death.
Glutathione Experts | What is Glutathione (GSH)?
| Glutathione Articles |
GSH FAQs
| GSH & Diseases |
Contact
