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[Increased ATP-hydrolase activity of the brain mitochondria under the effect of aminazine (electron cytochemical
Abstract:
The localization of Mg-stimulated ATPase activity was determined in the sensomotor cortex mitochondria of Wag rats after aminazin administration (15 mg/kg). Apart from normal mitochondria containing no reaction product, a number of altered mitochondria with different localization in them of the ATPase reaction product were recorded. The intact animals showed no sediment in the mitochondria. It is suggested that aminazin-induced increase in ATP-hydrolase activity is caused by two factors: neuroleptic-induced decrease in glycolytic and oxidative cell activity and increased permeability of mitochondrial membranes.
Insights
Aminazine administration altered Mg-stimulated ATPase activity in rat brain mitochondria. This neuroleptic drug increased ATP-hydrolase activity by reducing cell energy production and increasing mitochondrial membrane permeability.
Area of Science:
- Biochemistry
- Neuropharmacology
- Cell Biology
Context:
- Mitochondria play a crucial role in cellular energy metabolism.
- Neuroleptics are a class of drugs used to manage psychosis.
- ATPase activity is vital for cellular energy production.
Purpose:
- To investigate the effect of aminazine on Mg-stimulated ATPase activity in rat sensomotor cortex mitochondria.
- To understand the mechanisms underlying aminazine's impact on mitochondrial function.
Summary:
- Aminazine (15 mg/kg) administration to Wag rats altered the localization of Mg-stimulated ATPase activity in sensomotor cortex mitochondria.
- Altered mitochondria showed varied distribution of the ATPase reaction product, unlike intact animals.
- The study suggests aminazine increases ATP-hydrolase activity by decreasing glycolytic and oxidative cell activity and enhancing mitochondrial membrane permeability.
Impact:
- Provides insights into the neuropharmacological effects of aminazine on brain mitochondria.
- Contributes to understanding the cellular mechanisms of neuroleptic drug action.
- Highlights the potential for aminazine to disrupt mitochondrial energy homeostasis.