In an experiment conducted at Emory University in Atlanta, neurologists implanted osmotic pumps in 25 laboratory rats to continuously administer small doses of rotenone over a period of five weeks. The rotenone was dissolved in dimethyl sulfoxide (DMSO) and polyethylene glycol (PEG). Twelve of the 25 rats developed symptoms of Parkinsonís disease, including limb tremors and rigidity and examinations revealed that large numbers of dopamine producing cells in the ratsí brains had died or were damaged. The neurones of the substantia nigra in the brain also showed fibrous protein deposits that closely resemble Lewy bodies.
The results of this study do not, however, prove conclusively that rotenone causes Parkinsonís disease in humans because the method of administration was unnatural. The rotenone was continuously administered through the rat's jugular vein and it was mixed with DMSO and PEG. DMSO enhances tissue penetration of many chemicals.
Direct injection is the fastest way to introduce a chemical into the bloodstream, and in this study, the rats had continuously high levels of rotenone in their bloodstream. Normal exposure of humans to rotenone through use as an insecticide or piscicide would be ingestion, inhalation or through the skin and these significantly slow down the introduction of chemicals into the bloodstream. Also, most people using the chemical wear protective clothing, further minimising the risk of exposure. Generally, rotenone exposure is extremely limited due to the fact that it decomposes easily in the environment and in mammals and birds, rotenone is oxidised in the gut and excreted by the liver and kidneys, making it extremely unlikely that it would reach the substantia nigra in the brain. However, this does not mean that rotenone is safe, as it has been known to cause other side-effects such as vomiting and convulsions and in 1986 there was a case of fatal rotenone poisoning in a three and a half year old girl.
This research has opened up a more worrying prospect as rotenone works in a similar way to many other synthetic pesticides used widely in food production but which do not break down as easily. A classic symptom of exposure to widely used organophosphorus pesticides is muscle tremor, which is also a symptom of Parkinson's. There is therefore a possibility that chronic exposure to environmental toxins is linked to the incidence of Parkinson's disease and other degenerative diseases.
However, the real benefit of this study is that a new model of Parkinson's disease has been found. MPTP, as mentioned before, only induced Parkinson's-like symptoms in primates whereas rotenone administered in this manner should induce these symptoms in all mammals. This new model gives researchers a better method to study the cellular defects associated with Parkinson's disease and test potential treatments.