ABSTRACT
Propineb is a fungicide with a propylene-bis-dithiocarbamate structure. Pregnant Wistar rats were exposed to 400 ppm propineb concentrations in 5 ml distilled water, 5 days per week until the end of pregnancy. The rats were treated with propineb for 16 days and the brains of litter rats were sacrificed at first day of birth after which their brains were collected. Ultrastructural examination of the brains of the fetuses and propineb-treated pregnant females revealed a variety of histopathological effects. We suggest that mitochondrial damage may be an effective factor for neuron necrosis. These results supported the proposal that the exposure to fungicides such as propineb and to other naturally occurring compounds which inhibit mitochondrial function, may contribute to Parkinson's disease development.
El Propineb es un fungicida con una estructura de propileno-bis-ditiocarbamato. Ratas Wistar preñadas fueron expuestas a concentraciones de depropineb (400 ppm) en 5 ml de agua destilada, 5 días por semana hasta el final de la preñez. Las ratas fueron tratadas por 16 días y las crías fueron sacrificados el primer día de nacimiento para recolectar sus cerebros. El examen ultraestructural de los cerebros de los fetos y las hembras preñadas tratadas con propineb reveló una variedad de efectos histopatológicos. Sugerimos que el daño mitocondrial puede ser un factor eficaz para la necrosis neuronal. Estos resultados apoyaron la propuesta de que la exposición a los fungicidas tales como propineb y de otros compuestos de origen natural que inhiben la función mitocondrial, puede contribuir al desarrollo de la enfermedad de Parkinson.
Subject(s)
Animals , Female , Pregnancy , Rats , Zineb/analogs & derivatives , Zineb/pharmacology , Brain/drug effects , Brain/ultrastructure , Microscopy, Electron , Rats, WistarABSTRACT
Mancozeb, a commonly used fungicide, has been shown to induce tumours in mouse skin and maneb, unit constituent of mancozeb, is reported to induce tumours in rats. The mechanism by which mancozeb induced tumorigenicity is not known. Since the levels of inositol phospholipids and phosphatidic acid have roles in the regulation of cell proliferation, the effects of mancozeb on the levels of these lipids were studied in rats. Daily oral administration of commercial grade mancozeb at a concentration of 50 mg/kg body wt for 30 days (5 days a week) caused no significant change in the levels of inositol phospholipids and phosphatidic acid (PA) in both cerebrum and liver, while at high concentration (250 mg/kg body wt) under the same treatment schedule mancozeb increased the levels of these lipids. In cerebrum, the levels of phosphatidylinositol (PI) and PA were increased by 36 and 43% respectively without affecting the levels of polyphosphoinositides, whereas in liver the levels of not only PI (50%) and PA (49%) but also those of polyphosphoinositides were increased. These results show that mancozeb influences the levels of PA and inositol phospholipids, involved in phospholipase C-pathway of signalling.