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Oxidative Stress, Mitochondrial Respiration, and Parkinson's Disease
Author(s) -
COHEN GERALD
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06180.x
Subject(s) - oxidative stress , monoamine oxidase , mitochondrion , dopamine , respiration , chemistry , oxidative phosphorylation , parkinson's disease , neurotransmitter , biochemistry , medicine , endocrinology , biology , disease , enzyme , anatomy , receptor
A bstract : When either oxidizing species, such as H 2 O 2 or oxy‐radicals, are present in excess or cellular anti‐oxidant defenses are lowered, a state of oxidative stress exists. Parkinson's disease is characterized by the loss of dopamine (DA) neurons, which leads to overactivity of the surviving DA neurons and an increase in neurotramsmitter release and turnover. The increased metabolism of DA neurotransmitter by monoamine oxidase (MAO) can be looked upon as an endogenous oxidative stress, leading to damage to Complex I‐linked mitochondrial respiration. It remains an open question to what extent the mitochondrial damage seen in Parkinson's disease is of genetic origin and how much is caused by H 2 O 2 generated during enhanced turnover of DA, especially during treatment with L‐dopa.