Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytoplasmic (c) and mitochondrial (m) isoenzymes of aspartate aminotransferase (AAT, EC 2.6.1.1.) were isolated from rat heart extracts by electrophoresis in agar gel. Their pH optima and Km values were estimated; optimal conditions for estimation of the enzymatic activities are reported. Isadrine activated and adrenaline inhibited the cAAT activity. Noradrenaline did not affect the activity of both isoenzymes. Phentolamine, as contrary to obsidane which decreased the activity of both isoenzyme, activated the isoenzymes; the effect was partially decreased by obsidane. Phentolamine did not alter the noradrenaline effect on either mAAT or cAAT; it decreased significantly the free form of the mAAT activity only. Results of the experiments with administration of adrenomimetic drugs suggested that adrenaline and noradrenaline-isadrine had different sites of attachment through which they mediated their action on aspartate aminotransferase in rat heart mitochondria.
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PMID:[Role of adrenoreceptors in regulating aspartate aminotransferase isoenzyme activity in albino rat hearts]. 2 53

Cytoplasmic (c) and mitochondrial (m) isozymes of aspartate aminotransferase (AAT) (EC 2.6.1.1) were isolated from white rat liver tissue by means of electrophoresis in agar gel. For the enzymes Km values, pH optima were estimated and conditions, suitable for the reaction, were studied. On the basis of activating effectiveness on c-AAT the catecholamines were arranged in decreasing order as follows: adrenaline, isadrine, noradrenaline. Towards the m-AAT the series was: noradrenaline, isadrine, adrenaline. Obsidane decreased the action of adrenaline more effectively than it did isadrine. Phentholamine did not alter the effect of noradrenalin on c-AAT, but distinctly decreased the m-AAT activity. Beta-adrenergic receptor, but not alpha-receptor, participated in regulation of the AAT isozymes activity. Adrenaline promoted and isadrine inhibited the penetration of m-AAT into cytoplasma. Obsidane increased the effect of these catecholamines. After administration of phentholamine an increase in the AAT activity was caused by an increase in content of catecholamines in the organism.
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PMID:[Role of adrenergic mechanisms in the regulation of aspartate aminotransferase isoenzyme activity in the liver of white rats]. 102 34

In patients with unexplained pain after cholecystectomy, morphine often induces pain and may increase plasma aspartate aminotransferase activity because of exaggerated or prolonged rises in pressure within the biliary system. Previous studies have demonstrated that patients showing increases in aspartate aminotransferase have increases in plasma concentrations of noradrenaline and dopamine prior to and soon after induction of pain. The purpose of this study was to assess sympathetic activity under basal conditions in patients with (responders) and without (non-responders) increases in aspartate aminotransferase after challenge with morphine. When compared to non-responders, morphine responders had higher plasma concentrations of noradrenaline (p = 0.0001) and dopamine (p = 0.02) and higher urinary excretion of noradrenaline over 24 h (p = 0.03). Plasma and urinary levels of adrenaline were similar in the two groups. These observations indicate higher basal levels of sympathetic activity in the subgroup of patients showing increases in aspartate aminotransferase after challenge with morphine.
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PMID:Morphine responders with unexplained pain after cholecystectomy may have sympathetic overactivity. 182 68

The effect of differences in sympathoadrenomedullary and pituitary-adrenocortical responses of individual animals to 35% hemorrhage on severity of shock induction has been studied in unanesthetized unrestrained rats by measuring plasma concentrations of adrenaline (A), noradrenaline (NA), corticosterone (CS) and adrenocorticotropin (ACTH). The responses of A, CS and ACTH were related to the decrease of blood volume and mean arterial pressure (MAP), whereas plasma NA remained unchanged. Higher susceptibility to blood loss was characterized by more pronounced hemorrhage-induced increase in blood lactate concentration and plasma enzyme activities as well as lethal outcome of hemorrhagic shock. In animals with irreversible hemorrhagic shock, enhanced catecholamine secretion and reduced ACTH release was observed. Furthermore, a revealed direct correlation between A and blood lactate concentration and plasma enzyme activities (aspartate aminotransferase, isocitric dehydrogenase, creatine kinase, lipase and glutathione-S-transferase) may indicate its possible participation in the mechanism of shock induction. In contrast, an inverse relationship of plasma CS to the indicators of shock severity was demonstrated. In conclusion, non-optimal neuroendocrine regulation of cardiovascular adjustments to hemorrhage in shock-prone animals might cause an exaggerated compensatory activation of adrenomedullary catecholamine secretion, which in turn has been shown to exert deleterious vascular and metabolic effects. The mechanisms responsible for reduced ACTH secretion in shock-prone animals remain to be established.
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PMID:Hormonal responses to hemorrhage and their relationship to individual hemorrhagic shock susceptibility. 216 2

In patients with biliary type pain after cholecystectomy, morphine often precipitates pain and may induce rises in plasma concentrations of liver enzymes because of exaggerated or prolonged rises in intrabiliary pressure. In this study, changes in plasma concentrations of catecholamines and histamine were determined after the administration of morphine in patients with and without a two-fold or greater rise in the plasma concentration of aspartate aminotransferase at four hours. Those showing rises in aminotransferase had higher concentrations of noradrenaline at 40 and 60 minutes after morphine and higher concentrations of dopamine at 40 minutes after morphine. The two groups had similar concentrations of adrenaline and histamine. Attempts to inhibit rises in aminotransferase after morphine by pretreatment with histamine, serotonin and alpha-receptor blockers were largely unsuccessful, although inhibition was observed with phenoxybenzamine in two of five patients. Higher plasma concentrations of noradrenaline and dopamine before and soon after induction of pain in patients showing rises in aminotransferase are consistent with sympathetic activation but heterogeneity appears to exist in the response to alpha-receptor blockade.
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PMID:Sympathetic activation: a mechanism for morphine induced pain and rises in liver enzymes after cholecystectomy? 231 82

Determinants of plasma glucose concentrations were studied in patients on admission to hospital with confirmed acute myocardial infarction but without previous glucose intolerance as evidenced by raised concentrations of glycosylated haemoglobin (HbAlc). Mortality in hospital increased significantly with increasing plasma concentrations of glucose in patients with both normal (p less than 0.0001, n = 311) and borderline (p less than 0.02, n = 70) concentrations of HbAlc. There was a weak relation between plasma glucose concentrations and infarct size as estimated by peak aspartate transaminase activity in both HbAlc groups (rs = 0.26, n = 101 and rs = 0.41, n = 35 respectively). A correlation was found between adrenaline and plasma glucose concentrations (r = 0.47, n = 27) and cortisol and plasma glucose concentrations (r = 0.75, n = 19), but the relation of plasma noradrenaline and plasma glucose suggested a threshold effect. Concentrations of adrenaline, but not those of noradrenaline or cortisol, correlated with infarct size as measured both by peak aspartate transaminase activity and cumulative release of creatine kinase MB isoenzyme. Multiple regression analysis showed that concentrations of cortisol, adrenaline, and noradrenaline (but not the concentration of HbAlc, infarct size, or age) are the main determinants of plasma glucose concentration measured in non-diabetic patients when admitted to hospital after acute myocardial infarction.
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PMID:Determinants and importance of stress hyperglycaemia in non-diabetic patients with myocardial infarction. 309 14

This study describes the carioprotective effect of ceruloplasmin (CAS 9031-37-2) against oxygen free radical injury, as indicated by several biochemical indicators and some cardiodynamic variables. Isolated rat hearts (n = 4-8, p < 0.05, for each experimental point) in Langendorff preparation were exposed to oxygen free radicals generated by electrolysis (10 mA) in the absence and the presence of 0.25 mumol/l purified ceruloplasmin and denaturated ceruloplasmin, in Krebs-Henseleit perfusion solutions. Biochemical indicators (noradrenaline, malondialdehyde, creatine-kinase, lactate dehydrogenase, aspartate aminotransferase, Ca2+ and Mg2+) as well as the electrocardiogram and the left ventricular pressure (LVP), were altered by oxygen free radicals formation, denoting major cellular and tissular damages in the nontreated hearts. Ceruloplasmin exhibited a cardioprotective effect and prevented the oxygen free radical-induced release of noradrenaline, indicating that it can also protect the sympathetic nerve endings from oxygen free-radical injury. Purified ceruloplasmin, a circulating extracellular antioxidant and oxygen free radical scavenger, seems to be an effective heart protective agent against myocardial and neuronal injuries generated by oxygen free radicals.
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PMID:Protection of myocardial tissue against deleterious effects of oxygen free radicals by ceruloplasmin. 777 45

Anomalous responses to morphine are common in patients with unexplained pain in the upper abdomen after cholecystectomy and may be linked to activation of the sympathetic nervous system. The hypothesis that sympathetic suppression would attenuate anomalous responses to morphine was tested by a randomized, cross-over trial using a standard challenge with morphine, with and without pretreatment with clonidine (300 micrograms orally, 1 h prior to the administration of morphine). In 13 of the 15 patients who completed the study, pre-treatment with clonidine decreased plasma concentrations of noradrenaline, dopamine and adrenaline by 56, 15 and 25% respectively. This was associated with a significant reduction in morphine-induced pain (p = 0.02) and nausea (p = 0.04) and attenuated increases in plasma aspartate aminotransferase (AST) activity (p = 0.03). Clonidine attenuates anomalous responses to morphine, perhaps through effects on sympathetic nervous activity or plasma concentrations of catecholamines.
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PMID:Sympathetic suppression attenuates anomalous responses to morphine in unexplained pain after cholecystectomy. 784 98

We examined the kinetics study of serum enzyme after the administration of beta-blocking agents or alpha-stimulator in the experimental rats. Following the administration of beta-blocking agents, propranolol and pindolol, the serum levels of adenylate kinase, aldolase, lactate dehydrogenase and aspartate aminotransferase as well as that of creatine kinase increased in rats. The same was observed following the administration of noradrenaline (an alpha-stimulator). Isoenzyme pattern indicated that most of these enzymes were considered to be released from muscular tissues. There were also changes in serum calcium, inorganic phosphorus and magnesium, concurrently with the release of the enzymes into the serum.
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PMID:Effects of beta-blocking agents on the release of various enzymes in muscular tissues. 796 81

Effects of electrical stimulation of the hepatic nerves on acute liver damage were examined using isolated rat liver perfused in situ, 24 hours after intraperitoneal injection with D-galactosamine (800 mg/kg). The leakage of lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) from the liver was used as markers of acute liver damage. In perfused livers after treatment with galactosamine, nerve stimulation (20 V, 20 Hz, 2 ms) increased the leakage of LDH and AST about 3-fold over the basal level accompanied by the decrease in flow rate, whereas with control livers the leakage of LDH and AST into the effluent was almost undetectable throughout the perfusion. The rapid increase in the leakage of LDH and AST was observed during nerve stimulation even under conditions where perfusion flow was maintained constant. Such effects of hepatic nerve stimulation on galactosamine-treated livers were mimicked well by infusion of noradrenaline or phenylephrine, and inhibited by the alpha1-antagonist bunazosin. Artificial reduction of perfusion flow alone did not induce the rapid leakage of LDH and AST into the effluent. On the other hand, low concentration (10 nmol/L) of noradrenaline only minimally decreased the flow rate but apparently augmented liver cell damage. The acute liver damage augmented by noradrenaline was dependent on extracellular Ca2+. These results indicate that in the liver, already having been injured slightly, the activation of hepatic sympathetic nerves and circulating catecholamines exaggerates acute liver damage through an action on liver cells, which depends on the influx of extracellular Ca2+.
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PMID:Exaggeration of acute liver damage by hepatic sympathetic nerves and circulating catecholamines in perfused liver of rats treated with D-galactosamine. 861 32


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