[The effect of chronic acidosis on the activity of renal glutamate decarboxylase and GABA-transaminase].
Chronic acidosis evoked by a 7-day application of ammonium chloride in concentration of 2% increased the activity of glutamate decarboxylase (GAD) in renal homogenates of rats to approximately 160%. The enzyme activators, chlorides and adenosine triphosphate influenced in varying measures the GAD activity in renal homogenates of both controlled and acidotic animals. Whilst ATP was gradually loosing the activating effect, chlorides preserved it. The renal GAD is firmly bound on insoluble structures. The increase in GAD activity due to acidosis was accompanied by increasing permanence of this bind. After the substitution of ammonium chloride by drinking water, the return of the increased GAD activity to previous normal values lasted 7 days, whilst apparent normalization of the weight of experimental animals reoccurred on the first day. Subfractionation of the crude renal mitochondrial fraction by use of enzyme markers localized GAD in mitochondria. In renal homogenates the activities of GABA-transaminases were assessed. GABA-alpha-ketoglutarate transaminase was 5x more active than GABA-pyruvate transaminase. Acidosis resulted in augmentation of both transaminases--the first to 130%, the second to 160%. (Tab. 5, Fig. 3, Ref. 25.)
Turský
T
T
Ustav lekárskej chémie, biochémie a klinickej biochémie LFUK, Bratislave.
Lassánová
M
M
Pavlakovicová
K
K
D000612:4-Aminobutyrate Transaminase / Q000378:metabolism*; D000138:Acidosis / Q000201:enzymology*; D000818:Animals; D002908:Chronic Disease; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D066298:In Vitro Techniques; D007672:Kidney Cortex / Q000201:enzymology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar
D000612:4-Aminobutyrate Transaminase; D005968:Glutamate Decarboxylase
Vplyv chronickej acidózy na aktivitu oblickovej dekarboxylázy glutamátu a GABA-transamináz.