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Vitamin E supplements fail to protect mice from acute MPTP neurotoxicity
L Gong1, E A Daigneault, R V Acuff
1Department of Pharmacology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City 37614.
Abstract:
The effect of chronic treatment with vitamin E (VE) on acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity, as assessed by striatal dopamine (DA) depletion, was studied. Male C57B1/6J mice were fed VE (48 mg kg-1 per day, intragastric) for 4, 8, or 12 weeks prior to administration of MPTP (20 mg kg-1, i.p. x 3, 2 h intervals) or its diluent. Brain VE concentration was increased by exogenous supplements for 12 weeks. Striatal DA content was reduced by 85% to 90% after MPTP in control and VE-treated mice. Mice with elevated cerebral VE were not protected from MPTP toxicity, with DA content as an indicator. In conclusion, these findings indicate that moderate elevation of brain VE is not adequate for protecting DA-containing neurons against the toxic actions of a high dose of MPTP.
Insights
Chronic vitamin E (VE) supplementation did not protect mice from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity. Elevated brain VE levels did not prevent dopamine depletion in mice treated with MPTP.
Area of Science:
- Neuroscience
- Neuropharmacology
- Toxicology
Background:
- 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin that selectively destroys dopaminergic neurons, serving as a model for Parkinson's disease.
- Vitamin E (VE) is an antioxidant that may offer neuroprotection against oxidative stress implicated in neurodegenerative processes.
Purpose of the Study:
- To investigate the neuroprotective effects of chronic vitamin E (VE) treatment against acute MPTP-induced neurotoxicity in a mouse model.
- To determine if elevated brain VE concentrations can prevent striatal dopamine (DA) depletion caused by MPTP.
Main Methods:
- Male C57B1/6J mice received daily intragastric vitamin E (48 mg/kg) for 4, 8, or 12 weeks.
- MPTP (20 mg/kg) or its diluent was administered intraperitoneally at 2-hour intervals.
- Striatal dopamine (DA) content was measured as an indicator of neurotoxicity.
Main Results:
- MPTP administration significantly reduced striatal DA content by 85%–90% in both control and VE-treated groups.
- Chronic VE supplementation, even for 12 weeks, did not prevent the substantial depletion of DA following MPTP exposure.
- Brain VE concentrations were confirmed to be elevated in supplemented mice.
Conclusions:
- Moderate elevation of brain vitamin E is insufficient to protect dopaminergic neurons from the toxic effects of a high dose of MPTP.
- These findings suggest that VE, under these conditions, does not provide adequate neuroprotection against MPTP-induced dopaminergic neurotoxicity.