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ShareMar. 29, 2000 — Phenomenon long known, never before explained
SAN FRANCISCO, March 27 -- For the first time, scientists have identified a chemical in tobacco that may explain why smokers are statistically less vulnerable to Parkinson's disease. The compound has been shown to slow the breakdown of key brain chemicals, including dopamine, which is typically depleted in the brains of patients with Parkinson's disease, according to researchers at Virginia Tech. The association between smoking and Parkinson's disease has been known for more than 20 years, but until now could not be scientifically explained.
The findings were presented here today at the 219th national meeting of the American Chemical Society, the world's largest scientific society, by Kay Castagnoli, a senior research associate in the Department of Chemistry and a member of the school's Harvey W. Peters Center for the Study of Parkinson's Disease.
The tobacco compound is described as a derivative of naphthoquinone, and works by interfering with an enzyme in the brain known as monoamine oxidase (MAO). MAO typically breaks down neurotransmitters - including dopamine, serotonin, and norepinephrine - as part of normal chemical activity in the brain.
In their study, the Virginia Tech researchers administered MPTP, a designer drug that produces a Parkinson-like disease, to laboratory rodents. Sold in the early l980s, MPTP was meant to mimic the effects of heroin. Addicts who took large doses suffered severe Parkinsonian symptoms. The naphthoquinone derivative protected the rodents against the toxic effects of MPTP, according to the researchers.
The researchers have started a second rodent study to confirm their initial findings. In addition, tests are underway in which the blood platelets of smokers are examined - before and after they smoke - to see if the naphthoquinone or related tobacco-derived compounds reduce MAO activity. The results will be correlated with the effects of the napththoquinone on MAO activity in the rodent brain.
In another paper at the same meeting, Joanna S. Fowler, Ph.D., a scientist at Brookhaven National Laboratory, Upton, N.Y., reported that positron emission tomography (PET) studies show that smokers' brains have lower levels of MAO than non-smokers' brains. MAO is responsible for breakdown of dopamine, norepinephrine and serotonin, neurotransmitters that- control much of the brain's neuronal activity. This makes MAO a prime target for the development of drugs to treat both Parkinson's disease and depression, she said. Fowler added that the discovery that tobacco contains an MAO inhibitor suggests that smoking also may reduce depression - another reason why smokers find it so difficult to quit.
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