Invited Symposium: Quinones and Other Reactive Oxygen Species in Neurobiologic, Apoptotic, and Neurotoxic Processes
Parkinson's disease is a neurodegenerative disease that is secondary to the loss of dopamine cells. These abnormalities are thought to be due to increased free radical production during the metabolism of catecholamines. The antiapoptotic agent, bcl-2, has been shown to protect cells against the ravages of free radicals. The presentation deals with the test of the idea that bcl-2 could attenuate the toxic effects of DA on immortalized neural cells. Our findings demonstrate that DA caused dose-dependent cell death. The use of confocal microscopy and of flow cytometry showed that DA can cause apoptosis. Moreover, DA caused a marked increase in the production of reactive oxygen species in these cells. The overproduction of bcl-2 caused significant protection against DA-induced apoptosis. When taken together with similar demonstration that methamphetamine-induced toxicity was also attenuated by bcl-2 overexpression, these results provide support for a role of bcl-2 dysfunction in the development of dopamine system degeneration.
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|Cadet, J.L.; (1998). Free Radicals And Dopamine System Degeneration. 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/cadet0497/index.html|
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