Invited Symposium: Quinones and Other Reactive Oxygen Species in Neurobiologic, Apoptotic, and Neurotoxic Processes
Melamed, E (Neurology Dept and Felsenstein Medical Research Center, Rabin Medical Center, Israel)
Our knowledge of the factors that contribute to the pathogenesis of the selective degeneration of the dopaminergic neurons and the mechanism of cell death improved significantly. A mark increase of lipid peroxidation, protein oxidation and oxidative damage in DNA was observed in the Parkinsonian substantia nigra (SN). Although reduction in GSH, mitochondrial dysfunction, excess nitric oxide formation and inflammatory process are also suggested to be associated with the pathogenesis of Parkinson's disease (PD), they may all occur as a result of the increased oxidative stress. Dopamine, the local natural neurotransmitter, and related catecholamines are hypothesis to contribute to the selective degeneration of dopaminergic neurons. Many in vitro studies have shown that catechols are potent toxin which are lethal to various cultured neuronal and non-neuronal cell. It was shown that these reagent induce typical apoptosis cell death both in neuronal cultures and in animal models of dopaminergic neuronal degeneration (i.e. MPTP and 6-OHDA). Moreover, several in-situ studies demonstrated the important of apoptotic cell death in the pathology of dopaminergic neurons in the SN of PD's patients. The accumulation data suggests possible avenues for providing neuroprotection through the reduction of oxidative stress via antioxidants or downstream the cell death process by to inhibiting apoptosis utilizing biochemical or genetic manipulations.
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|Offen, D; Melamed, E; (1998). The possible role of catecholamines toxicity in the nigrostriatal neuronal degeneration in Parkinson's disease. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/kostrzewa/offen0897/index.html|
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