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Journal ArticleDOI

Basal Lipid Peroxidation in Substantia Nigra Is Increased in Parkinson's Disease

TLDR
The results may indicate that an increased level of lipid peroxidation continues to occur in the parkinsonian nigra up to the time of death, perhaps because of continued exposure to excess free radicals derived from some endogenous or exogenous neurotoxic species.
Abstract
Polyunsaturated fatty acid (PUFA) levels (an index of the amount of substrate available for lipid peroxidation) were measured in several brain regions from patients who died with Parkinson's disease and age-matched control human postmortem brains. PUFA levels were reduced in parkinsonian substantia nigra compared to other brain regions and to control tissue. However, basal malondialdehyde (MDA; an intermediate in the lipid peroxidation process) levels were increased in parkinsonian nigra compared with other parkinsonian brain regions and control tissue. Expressing basal MDA levels in terms of PUFA content, the difference between parkinsonian and control substantia nigra was even more pronounced. Stimulating MDA production by incubating tissue with FeSO4 plus ascorbic acid, FeSO4 plus H2O2, or air alone produced lower MDA levels in the parkinsonian substantia nigra, probably reflecting the lower PUFA content. These results may indicate that an increased level of lipid peroxidation continues to occur in the parkinsonian nigra up to the time of death, perhaps because of continued exposure to excess free radicals derived from some endogenous or exogenous neurotoxic species.

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Citations
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Chronic systemic pesticide exposure reproduces features of Parkinson's disease

TL;DR: It is reported that chronic, systemic inhibition of complex I by the lipophilic pesticide, rotenone, causes highly selective nigrostriatal dopaminergic degeneration that is associated behaviorally with hypokinesia and rigidity.
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Neurodegenerative diseases and oxidative stress.

TL;DR: Oxidative stress has been implicated in the progression of Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis and different strategies, including novel metal–protein attenuating compounds aimed at a variety of targets have shown promise in clinical studies.
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Mitochondrial complex I deficiency in Parkinson's disease.

TL;DR: Results indicated a specific defect of Complex I activity in the substantia nigra of patients with Parkinson's disease, which 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.
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Oxidative stress hypothesis in alzheimer's disease

TL;DR: Supporting indirect evidence comes from a variety of in vitro studies showing that free radicals are capable of mediating neuron degeneration and death, suggesting that therapeutic efforts aimed at removal of ROS or prevention of their formation may be beneficial in AD.
Journal ArticleDOI

Oxidative stress in Parkinson's disease

TL;DR: Oxidative stress contributes to the cascade leading to dopamine cell degeneration in Parkinson's disease (PD), but oxidative stress is intimately linked to other components of the degenerative process, such as mitochondrial dysfunction, excitotoxicity, nitric oxide toxicity and inflammation.
References
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Journal Article

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Journal ArticleDOI

A simple method for the isolation and purification of total lipides from animal tissues.

TL;DR: In this paper, the authors described a simplified version of the method and reported the results of a study of its application to different tissues, including the efficiency of the washing procedure in terms of the removal from tissue lipides of some non-lipide substances of special biochemical interest.
Journal ArticleDOI

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Journal Article

Oxidative Pathways for Catecholamines in the Genesis of Neuromelanin and Cytotoxic Quinones

TL;DR: The autoxidation, periodate oxidation, and tyrosinase-mediated oxidation of 6-hydroxydopamine, dopamine, norepinephrine, and epinephrine were studied by absorption spectroscopy and gave evidence for a transient intermediate, the o -quinone, which rapidly tautomerized to the p-quinone.
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