Oxidative Stress and Parkinson Disease

Abstract

The cause of Parkinson disease is not known at present, and there are many theories as to why the loss of nerve cells that characterises the condition occurs. In recent years, there has been some interest in role of free-radical damage, particularly the damage caused by highly reactive molecules in Parkinson disease and other conditions. In early stages of Parkinsonism, there appears to be a compensatory increase in the number of dopamine receptors to accommodate the initial loss of dopamine neurons. As the disease progress, the number of dopamine receptors decreases, apparently due to concomitant degeneration of dopamine target sites on striatal neurons. The loss of dopaminergic neurons in Parkinson's disease results in enhanced metabolism of dopamine, augmenting the formation of H 2 O 2 , thus leading to generation of highly neurotoxic radicals (OH • ). It has been supposed that degeneration in Parkinson's disease could be a result from the oxidative stress due to dysregulation of dopamine metabolism with consequent free radical formation, depletion of reduced glutathione, a high level of total iron with reduced level of ferritin and deficiency of mitochondrial complex I.