RESUMO
The model of hyperenzymia caused by injection of lactate dehydrogenase (5000 U/kg body weight) causes an increase of NADP.H-dependent oxidation in liver microsomes, without changing oxidative intensity in mitochondria, by such NAD.H-depended dehydrogenases as glutamate dehydrogenase and beta-hydroxybutyrate dehydrogenase. The aim of the interaction with exogenous lactate dehydrogenase in the glycolytic metabolone system, where increased carbohydrate disintegration in vivo is induced. There is a high detoxification processes associated with ammonia detoxification and urea production. The stability of membrane permeability is characterized by the absence of glutamate dehydrogenase and glucoso-6-phosphate dehydrogenase activity in blood plasma. It has been shown that the introduction of exogenic lactate dehydrogenase into the metabolism of experimental animals gives the possibility of using this enzyme as an enzymotherapeutic remedy.
