[Increased ATP-hydrolase activity of the brain mitochondria under the effect of aminazine (electron cytochemical study)].
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.
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000201:enzymology*; D002746:Chlorpromazine / Q000494:pharmacology*; D006651:Histocytochemistry; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000201:enzymology* / Q000648:ultrastructure; D051381:Rats
D000251:Adenosine Triphosphatases; D008274:Magnesium; D002746:Chlorpromazine
Povyshenie ATF-gidrolaznoĭ aktivnosti mitokhondriĭ mozga pod vliianiem aminazina (elektronno-tstokhimicheskoe issledovanie).