Oxidative stress, mitochondrial respiration, and Parkinson's disease

Abstract

When either oxidizing species, such as H2O2 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 neurotransmitter 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 H2O2 generated during enhanced turnover of DA, especially during treatment with L-dopa.