Depletion of copper and manganese in brain after MPTP treatment of mice.
The mechanism of action of MPTP, a parkinsonism-inducing drug has been related to trace metals as a result of the observed potentiation of the neurotoxic action of the drug when diethyldithiocarbamate is concurrently administered. Diethyldithiocarbamate is a well-known chelator of trace metals, particularly copper. In the present study we analyzed the concentrations of copper and manganese in four brain regions of mice treated with neurotoxic doses of MPTP, in order to further substantiate the relationship between trace metals of MPTP-induced neurotoxicity. Male Swiss albino mice were administered with MPTP (30 mg/kg) for either three or five days. Seven days after the last MPTP administration, they were sacrificed and the content of manganese and copper in the following regions was determined by graphite furnace atomic absorption spectrophotometry: cortex, cerebellum, midbrain and corpus striatum. Results indicate a significant depletion of manganese in corpus striatum (19.5% versus control) in the mice treated with MPTP for 5 days. Copper was also found to be decreased in corpus striatum (17.3% in mice treated for 3 days and 51.3% in mice treated for 5 days). Midbrain copper was depleted by 42.9% in the group of mice treated for 5 days with MPTP. Results indicate that MPTP induced a diminution of both copper and manganese in corpus striatum, suggesting that this alteration could be related to MPTP mechanism of action.
D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects*; D003300:Copper / Q000172:deficiency*; D015259:Dopamine Agents / Q000633:toxicity*; D020267:MPTP Poisoning; D008297:Male; D008345:Manganese / Q000172:deficiency*; D051379:Mice; D009498:Neurotoxins / Q000633:toxicity
D015259:Dopamine Agents; D009498:Neurotoxins; D008345:Manganese; D003300:Copper