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Effects of nerve growth factor on antioxidative system in the thalamus of MPTP treated Wistar rats
M B Ninković1, M D Jovanović, Z Malicević
1Military Medical Academy, Institute for Medical Research, Belgrade.
Abstract:
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism is one of the most useful models for the study of that disease. It has been suggested that MPTP-induced neurotoxicity may involve the production of reactive oxygen species. MPTP was applied intracerebrally, unilaterally, in the striatum in single dose of 0.09 g/kg b.w. The second group was treated both with MPTP and nerve growth factor (NGF) in dose of 7 ng/ml. NGF was applied immediately after the neurotoxin. Control group was treated with 0.9% saline solution in the same manner. Animals were decapitated 7 days after the treatment. In the group treated with MPTP, the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) was decreased in ipsilateral thalamus, compared to control values as well as to the contralateral thalamus. In the same structures superoxide anion production was increased, compared to controls. Following the application of both MPTP and NGF, the activity of SOD and GSH-Px remained on control values, while the superoxide anion content was decreased, compared to controls. These results indicate a temporal and spatial propagation of oxidative stress and spread protective effects of NGF on the thalamus, the structure that is distant, but very tightly connected with striatum, the place of direct neurotoxic damage.
Insights
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes parkinsonism by increasing oxidative stress. Nerve growth factor (NGF) protected against MPTP-induced damage in the thalamus, suggesting a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a widely used neurotoxin to model Parkinson's disease.
- MPTP-induced neurotoxicity is hypothesized to involve reactive oxygen species (ROS).
Purpose of the Study:
- To investigate the role of oxidative stress in MPTP-induced parkinsonism.
- To evaluate the neuroprotective effects of nerve growth factor (NGF) against MPTP toxicity.
Main Methods:
- MPTP was administered intracerebrally to the striatum in rats.
- Nerve growth factor (NGF) was co-administered with MPTP in a separate group.
- Control group received saline.
- Enzyme activities (superoxide dismutase, glutathione peroxidase) and superoxide anion production were measured in the thalamus 7 days post-treatment.
Main Results:
- MPTP treatment significantly decreased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity and increased superoxide anion production in the ipsilateral thalamus.
- Co-administration of NGF with MPTP maintained SOD and GSH-Px activity at control levels and reduced superoxide anion production.
- Oxidative stress markers showed propagation from the striatum to the connected thalamus.
Conclusions:
- MPTP induces oxidative stress in the thalamus, indicating a spread of damage beyond the direct site of administration.
- Nerve growth factor (NGF) demonstrates significant neuroprotective effects against MPTP-induced oxidative stress in the thalamus.