Insecticide Exposure in Parkinsonism.
Annual rept. 1 Jan-31 Dec 99
VIRGINIA POLYTECHNIC INST AND STATE UNIV BLACKSBURG
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A series of behavioral, neurochemical, and immunocytochemical studies were undertaken to characterize the possible role of insecticide exposure in the etiology of Parkinsons disease as it may relate to Gulf War Syndrome. The insecticides under study are the organophosphorus compound chlorpyrifos and the pyrethroid, permethrin given 3 times over a two week period by injection chlorpyrifos subcutaneous and permethrin intraperitoneal. Permethrin showed an up-regulation of dopamine transport at a dose of 1.5 mgkg, which is at least two orders of magnitude below its LD50. At higher doses of permethrin -25 mgkg, the increase in transport declined to a level below that of control. Toxic effects may have been involved, since immunocytochemical labeling of the caudate-putamen found that transporter staining was near control levels. Both permethrin and chlorpyrifos caused small, but statistically significant decreases in mitochondrial dehydrogenase activity. However, cytotoxicity was not reflected in levels of striatal dopamine, which were not changed by 100 mgkg chlorpyrifos or 200 mgkg permethrin. There was, however, an increase in dopamine turnover at 100 mgkg chlorpyrifos, as indicated by a significant increase in titers of the dopamine metabolite, 3,4-dihydroxyphenylacetic acid. Chlorpyrifos at 25-100 mgkg caused 15-84 inhibition of acetylcholinesterase, which correlated reasonably well with effects on open field, rearing, and pole climbing behaviors. Permethrin caused a significant decline in open field behavior, which may have been related to a doubling of muscarinic receptor density in the striatum of mice treated with -50 mgkg. These studies demonstrate significant effects on dopamine neurochemistry by these insecticides.
- Medicine and Medical Research
- Stress Physiology