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Title: Glutathione in Parkinson’s disease: a link between oxidative stress and mitochondrial damage?
Author: Di Monte DA; Chan P; Sandy MS
Address: California Parkinson’s Foundation, San Jose 95128.
Source: Ann Neurol, ():
Several links exist between the two mechanisms of neuronal degeneration (i.e., oxygen radical production
and mitochondrial damage) proposed to have a role in Parkinson's disease. Indeed, mitochondria are
critical targets for the toxic injury induced by oxygen radicals, and experimental evidence suggests that
mitochondrial damage may cause an increased generation of oxygen radicals. A potentially important link
between these two mechanisms of neurodegeneration is glutathione. Because of the scavenging activity
of glutathione against accumulation of oxygen radicals, its decrease in the brains of parkinsonian patients
has been interpreted as a sign of oxidative stress; however, this change may also result from or lead to
mitochondrial damage. It is conceivable therefore that regardless of whether oxidative stress or
mitochondrial damage represents the initial insult, these toxic mechanisms may both contribute to
neuronal degeneration via changes in glutathione levels.
ISSN: 0364-5134
Title: Dopamine turnover and glutathione oxidation: implications for Parkinson disease.
Author: Spina MB; Cohen G
Address: Department of Neurology, Mount Sinai School of Medicine, City University of New York, NY
Source: Proc Natl Acad Sci U S A, 86(4):1398-400 1989 Feb
Parkinson disease is characterized by a major loss (approximately 80% or more) of dopaminergic
nigrostriatal neurons and by an increased turnover of neurotransmitter by surviving neurons of the
nigrostriatal tract. In theory, increased turnover of dopamine should be associated with an oxidative stress
derived from increased production of hydrogen peroxide. The peroxide is formed during the oxidative
deamination of dopamine by monoamine oxidase. In experiments with mice, increased presynaptic
turnover of dopamine was evoked by injection of reserpine, which interferes with the storage of dopamine
in synaptic vesicles. Loss of dopamine and formation of deaminated metabolites were accompanied by a
significant rise (87.8%) in the level of oxidized glutathione in brain. This change was observed in the
striatum, which is richly innervated by dopamine terminals, but not in the frontal cortex, which receives a
much sparser innervation by catecholamine nerve terminals. The rise in oxidized glutathione was seen
even though dopamine terminals constitute only 1% or less of the mass of the striatum. Clorgyline, an
inhibitor of monoamine oxidase type A, blocked the formation of oxidized glutathione. These
observations confirm that a selective increase in neurotransmitter turnover within nigrostriatal nerve
terminals can evoke a change in cellular redox status. We suggest that an oxidative stress may play a role
in the natural history of Parkinson disease.
Publication Type: JOURNAL ARTICLE
ISSN: 0027-8424
Title: Alterations in glutathione levels in Parkinson's disease and other neurodegenerative disorders
affecting basal ganglia [see comments]
Author: Sian J; Dexter DT; Lees AJ; Daniel S; Agid Y; Javoy-Agid F; Jenner P; Marsden CD
Address: Parkinson's Disease Society Experimental Research Laboratories, Pharmacology Group,
Biomedical Sciences Division, King's College London, UK.
Source: Ann Neurol, 36(3):348-55 1994 Sep
Reduced glutathione (GSH) and oxidized glutathione (GSSG) levels were measured in various brain
areas (substantia nigra, putamen, caudate nucleus, globus pallidus, and cerebral cortex) from patients
dying with Parkinson's disease, progressive supranuclear palsy, multiple-system atrophy, and
Huntington's disease and from control subjects with no neuropathological changes in substantia nigra.
GSH levels were reduced in substantia nigra in Parkinson's disease patients (40% compared to
control subjects) and GSSG levels were marginally (29%) but insignificantly elevated; there were no
changes in other brain areas. The only significant change in multiple-system atrophy was an increase
of GSH (196%) coupled with a reduction of GSSG (60%) in the globus pallidus. The only change in
progressive supranuclear palsy was a reduced level of GSH in the caudate nucleus (51%). The only
change in Huntington's disease was a reduction of GSSG in the caudate nucleus (50%). Despite
profound nigral cell loss in the substantia nigra in Parkinson's disease, multiple-system atrophy, and
progressive supranuclear palsy, the level of GSH in the substantia nigra was significantly reduced
only in Parkinson's disease. This suggests that the change in GSH in Parkinson's disease is not solely
due to nigral cell death, or entirely explained by drug therapy, for multiple-system atrophy patients
were also treated with levodopa. The altered GSH/GSSG ratio in the substantia nigra in Parkinson's
disease is consistent with the concept of oxidative stress as a major component in the pathogenesis of
nigral cell death in Parkinson's disease.
Publication Type: JOURNAL ARTICLE
ISSN: 0364-5134
Title: Glutathione peroxidase in early and advanced Parkinson's disease.
Author: Johannsen P; Velander G; Mai J; Thorling EB; Dupont E
Address: Department of Neurology, University Hospital, Aarhus Kommunehospital, Aarhus, Denmark.
Source: J Neurol Neurosurg Psychiatry, 54(8):679-82 1991 Aug
A defective antioxidant scavenging system plays a major role in one of the theories of the
pathogenesis of Parkinson's disease. The aim of this study was to investigate whether there is a
general difference in antioxidant activity between early and advanced cases of Parkinson's disease.
Twenty five recently diagnosed patients, without any clinical fluctuations (group A), and 25 patients
in a late phase of the disease with severe fluctuations in response to levodopa therapy (group B) were
included in the study. Erythrocyte glutathione peroxidase was determined as a measure of antioxidant
activity and significantly lower values were found in group B than in group A. Regression analyses in
groups A and B showed significant correlation between glutathione peroxidase and duration of
disease, but not between glutathione peroxidase and age of patients.
Publication Type: JOURNAL ARTICLE
ISSN: 0022-3050
Title: Reduced intravenous glutathione in the treatment of early Parkinson's disease.
Author: Sechi G; Deledda MG; Bua G; Satta WM; Deiana GA; Pes GM; Rosati G
Address: Department of Neurology, University of Sassari, Italy.
Source: Prog Neuropsychopharmacol Biol Psychiatry, 20(7):1159-70 1996 Oct
1. Several studies have demonstrated a deficiency in reduced glutathione (GSH) in the nigra of
patients with Parkinson's Disease (PD). In particular, the magnitude of reduction in GSH seems to
parallel the severity of the disease. This finding may indicate a means by which the nigra cells could
be therapeutically supported. 2. The authors studied the effects of GSH in nine patients with early,
untreated PD. GSH was administered intravenous, 600 mg twice daily, for 30 days, in an open label
fashion. Then, the drug was discontinued and a follow-up examination carried-out at 1-month interval
for 2-4 months. Thereafter, the patients were treated with carbidopa-levodopa. 3. The clinical
disability was assessed by using two different rating scale and the Webster Step-Second Test at
baseline and at 1-month interval for 4-6 months. All patients improved significantly after GSH
therapy, with a 42% decline in disability. Once GSH was stopped the therapeutic effect lasted for 2-4
months. 4. Our data indicate that in untreated PD patients GSH has symptomatic efficacy and possibly
retards the progression of the disease. <
ISSN: 0278-5846
Title: Mitochondrial impairment as an early event in the process of apoptosis induced by glutathione
depletion in neuronal cells: relevance to Parkinson's disease.
Author: Merad-Boudia M; Nicole A; Santiard-Baron D; Saill´e C; Ceballos-Picot I
Address: CNRS URA 1335, CHU Necker-Enfants Malades, Paris, France.
Source: Biochem Pharmacol, 56(5):645-55 1998 Sep 1
In Parkinson's disease (PD), dopaminergic cell death in the substantia nigra was associated with a
profound glutathione (GSH) decrease and a mitochondrial dysfunction. The fall in GSH concentration
seemed to appear before the mitochondrial impairment and the cellular death, suggesting that a link
may exist between these events.The relationships between GSH depletion, reactive oxygen species
(ROS) production, mitochondrial dysfunction and the mode of cell death in neuronal cells remain to
be resolved and will provide important insights into the etiology of Parkinson's disease. An approach
to determine the role of GSH in the mitochondrial function and in neurodegeneration was to create a
selective depletion of GSH in a neuronal cell line in culture (NS20Y) by inhibiting its biosynthesis
with L-buthionine-(S,R)-sulfoximine (BSO), a specific inhibitor of gamma-glutamylcysteine
synthetase. This treatment led to a nearly complete GSH depletion after 24 hr and induced cellular
death via an apoptotic pathway after 5 days of BSO treatment. By using the reactive oxygen species-
sensitive probe 2',7'-dichlorofluorescin, we observed that the rapid GSH depletion was accompanied,
early in the process, by a strong and transient intracellular increase in reactive oxygen species
evidenced after 1 hr with BSO, culminating after 3 hr when the GSH level decreased to 30% of
normal. GSH depletion induced a loss of mitochondrial function after 48 hr of BSO treatment. In
particular, the activities of complexes I, II and IV of the respiratory chain were decreased by 32, 70
and 65%, respectively as compared to controls. These results showed the crucial role of GSH for
maintaining the integrity of mitochondrial function in neuronal cells. Oxidative stress and
mitochondrial impairment, preceding DNA fragmentation, could be early events in the apoptotic
process induced by GSH depletion. Our data are consistent with the hypothesis that GSH depletion
could contribute to neuronal apoptosis in Parkinson's disease through oxidative stress and
mitochondrial dysfunction.
Publication Type: JOURNAL ARTICLE
ISSN: 0006-2952



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