ABSTRACT
Acute cooling of rats led to stimulation of NAD+-dependent isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH) and NAD(P)+-transhydrogenase (TH) but did not affect the NADP+-ICDH activity in liver, heart and skeletal muscle mitochondria. After pretreatment of the animals with propranolol the stimulating effect was decreased, thus suggesting that endogenous catecholamines and beta-adrenoreceptors are of importance in activation of NAD+-ICDH, SDH and TH. The effects of cooling, noradrenaline and cAMP did not summarize. Role of catecholamines in stimulation of mitochondrial oxidative enzymes under conditions of cooling is discussed.
Subject(s)
Catecholamines/physiology , Cold Temperature , Mitochondria, Heart/enzymology , Mitochondria, Liver/enzymology , Oxygenases/metabolism , Stress, Physiological/enzymology , Animals , Enzyme Activation , Rats , Rats, Inbred Strains , Receptors, Adrenergic, beta/drug effects , Stress, Physiological/physiopathologyABSTRACT
Administration of noradrenaline in a dose of 11 mumol/kg activates succinate dehydrogenase (SDH) in the rat liver. On incubation of liver homogenate with noradrenaline (10(-6) M), cAMP (10(-6) M) and NaF (10(-2) M), a nonhormonal activator of adenylate cyclase, SDH was found to be activated by 20--30% in all the cases. The effects of noradrenaline and cAMP did not sum up. It seems likely that SDH activation by catecholamines is mediated by cAMP. Acute cooling (--17 degrees C) stimulates SDH via endogenous catecholamines, since this effect is completely reversed by the beta-adrenolytic inderal.