Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the absence of an exogenous energy source, galactose-grown cells of Streptococcus lactis ML3 rapidly accumulated thiomethyl-beta-D-galactopyranoside (TMG) and 2-deoxyglucose to intracellular concentrations of 40 to 50 mM. Starved cells maintained the capacity for TMG uptake for many hours, and accumulation of the beta-galactoside was insensitive to proton-conducting ionophores (tetrachlorosalicylanilide and carbonylcyanide-m-chlorophenyl hydrazone) and sulfydryl group reagents including iodoacetate and N-ethylmaleimide. Fluorimetric analysis of glycolytic intermediates in extracts prepared from starved cells revealed (a) high intracellular levels of phosphoenolpyruvate (13 mM; PEP) and 2-phosphoglycerate (approximately 39 mM; 2-PG), but an absence of other metabolites including glucose 6-phosphate, fructose 6-phosphate, fructose 1,6-diphosphate, and triosephosphates. The following criteria showed PEP (and 2-PG) to be the endogenous energy source for TMG accumulation by the phosphotransferase system: the intracellular concentrations of PEP and 2-PG decreased with concomitant uptake of TMG, and a close correlation was observed between maximum accumulation of the beta-galactoside and the total available concentration of the two intermediates; TMG accumulated as an anionic derivative, which after extraction and incubation with alkaline phosphatase (EC 3.1.3.1) formed the original analogue; fluoride inhibition of 2-phospho-D-glycerate hydrolyase (EC 4.2.1.11) prevented the conversion of 2-PG to PEP, and uptake of TMG by the starved cells was reduced by 80%; and the stoichiometric ratio [TMG] accumulated/[PEP] consumed was almost unity (0.93). In cells metabolizing glucose, all intermediates listed in (a) and (b) were found. Upon exhaustion of glucose from the medium, the metabolites in (b) were not longer detectable, while the intracellular concentrations of PEP and 2-PG increased to the levels previously observed in starved cells. The glycolytic intermediates in (b) are all in vitro heterotropic effectors of pyruvate kinase (adenosine 5'-triphosphate:pyruvate 2-O-phosphotransferase, EC 2.7.1.40) from S. lactis ML3. It is suggested that the capacity of starved cells to maintain high intracellular concentrations of PEP and 2-PG is a consequence of decreased in vivo activity of this key regulatory enzyme of glycolysis.
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PMID:Phosphoenolpyruvate and 2-phosphoglycerate: endogenous energy source(s) for sugar accumulation by starved cells of Streptococcus lactis. 12 9

Studies of the uteroplacental blood flow and of some peripheral blood enzymes activities in 117 pregnant women have revealed that deterioration of the uteroplacental blood flow is associated with an increase of the activities of hydroxybutyrate and lactate dehydrogenases, creatine phosphokinase, and alkaline phosphatase. Exhaustion of the compensatory adaptive mechanisms, that manifests itself by a marked reduction of the blood flow in the intervillous space and by an intrauterine fetal distress is paralleled by a reduction of these enzymes activities.
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PMID:[Relations between indicators of the activity of several blood enzymes and the state of the utero-placental blood flow in pregnant women at high risk of perinatal pathology]. 271 20

Batch cultures of Aspergillus niger grown from conidia on a medium with high C/N ratio accumulated gluconate from glucose with a yield of 57%. During almost the whole time of accumulation there was no net synthesis of total protein in the mycelium but the activity per flask and the specific activity of glucose oxidase (EC 1.1.3.4) in mycelial extracts increased whereas both values decreased for glucose dehydrogenase (EC 1.1.99.10) 'gluconate 6-phosphatase' (cf. EC 3.1.3.1, 3.1.3.2), gluconokinase (EC 2.7.1.12), glucose 6-phosphate and phosphogluconate dehydrogenases (EC 1.1.1.49, EC 1.1.1.44), phosphoglucomutase (EC 2.7.5.1), and most enzymes of the Embden-Meyerhof pathway and the tricarboxylic acid cycle. Gluconate dehydratase (EC 4.2.1.39), gluconate dehydrogenase (EC 1.1.99.3) and enzymes of the Entner-Doudoroff pathway could not be detected. By cycloheximide the increase of glucose oxidase activity was inhibited. It is concluded that the high yield of gluconate was due mainly to the net (de novo) synthesis of glucose oxidase which occurred during protein turnover after the exhaustion of the nitrogen source, and which was not accompanied by a net synthesis of the other enzymes investigated. Some gluconate may also have been formed by hydrolytic cleavage of gluconate 6-phosphate.
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PMID:Gluconate accumulation and enzyme activities with extremely nitrogen-limited surface cultures of Aspergillus niger. 301 15

In Channa punctatus exposed to a safe dose (4.5 ppm) of the commercial carbamate pesticide carbofuran for 6 months, from January to June, liver exhibited varying degrees of histopathological changes including cytoplasmolysis, nuclear pyknosis, and necrosis leading to complete exhaustion and disintegration of hepatocytes. In some regions of liver, extensive degeneration of proliferated hepatocytes, in close proximity to blood sinuses, looking like darkly stained debris of hepatomass and induction of tumors were indicative of carcinogenic action of this pesticide which may be attributed to its cumulative toxicity during chronic exposure. Apart from this, the rupturing of blood sinus causing invasive infiltration of leukocytes, and detrimental focal necrosis resulting in the complete dissolution of hepatocytes indicated by the presence of debris mass in the necrotic space can be seen. Moreover, in the liver of experimental fish, corresponding to cellular damage, a significant decrease in hepatosomatic index and ascorbic acid content and an elevation in acid and alkaline phosphatase levels were also recorded. These results suggest that carbofuran is capable of inducing histopathological and biochemical alterations in liver which may cause physiometabolic dysfunction in this species.
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PMID:Carbofuran-induced histopathological and biochemical changes in liver of the teleost fish, Channa punctatus (Bloch). 322 78

The action of somatostatin on intestinal alkaline phosphatase activity (IAP) in the duodenal juice was examined in 22 subjects undergoing diagnostic secretin-CCK-PZ-tests. Under continuous secretin-CCK-PZ-stimulation there is an increase of IAP which is followed by a period of exhaustion after 1 h of stimulation. The intravenous administration of somatostatin induces a distinct inhibition of IAP which cannot be due to the exhaustion of the enzyme synthesis. As there is a functional relationship between fat absorption and alkaline phosphatase, it is suggested that this inhibition of IAP is one of the mechanisms of the somatostatin-induced inhibition of intestinal fat absorption.
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PMID:The action of somatostatin on intestinal alkaline phosphatase stimulated by secretin and cholecystokinin-pancreozymin. 610 6

The authors examined biochemically and histochemically the activity of alkaline phosphatase and adenosinetriphosphatase in lymph nodules of experimental animals, living under the conditions of continuous noise action (3 and 5 months) at a level of 95 decibels A for 3 hours daily in the morning. There were phase changes in the activity of the examined enzymes, which revealed considerable stability even after stopping the contact of the organism with noise factor. The manifested inhibition of the activity of alkaline phosphatase and partly of adenosinetriphosphatase suggested that the cells of lymph tissue revealed disturbances in the metabolic processes, which caused exhaustion of their protective function.
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PMID:[Biochemical and histochemical studies of the alkaline phosphatase and adenosine triphosphatase levels in the lymph nodes of experimental animals after noise exposure]. 645 69

Blood samples were taken before and immediately after 80 km and 40 km rides held on consecutive days and analysed for haematocrit, blood glucose and lactate, plasma sodium, potassium, calcium, albumin, free fatty acids (FFA), glycerol, bicarbonate, insulin, cortisol, glucagon, urea, creatinine, uric acid, bilirubin and alkaline phosphatase. Unusually hot weather probably contributed to haemoconcentration with a significant (P < 0.001) increase in haematocrit and plasma albumin. A fall in blood glucose, with a rise in FFA and glycerol were consistent with long distance riding and were associated with a reduction in plasma insulin and a rise in cortisol and glucagon. The results suggested that the horses were working aerobically and the small increase in blood lactate was likely to be a result of reduced tissue perfusion. Plasma urea, creatinine and bilirubin increased during the 80 km ride and were still high the next morning. Blood samples were taken from 2 horses that became exhausted and were forced to retire and the results from these animals indicate the slow rate of recovery. It is suggested that haemoconcentration with reduced tissue perfusion might contribute to exhaustion during long distance exercise and that the speed of recovery might be improved by the intravenous administration of balanced electrolyte solutions.
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PMID:Further studies on the metabolic effects of long distance riding: Golden Horseshoe Ride 1979. 743 43

The effects of strenuous exercise on the mechanisms of bile formation were studied in rats. Animals (n = 8) were exercised to exhaustion in a rodent treadmill at a speed of 24 m/min and a 12% slope. Hepatic glutathione concentration was significantly reduced (-40%) and liver malondialdehyde content significantly increased (+37%) when compared to sedentary controls (n = 6). Both serum alkaline phosphatase level and bile acid concentration were significantly higher in runners (+81% and +85%). Bile flow and the biliary secretion of bile acids were significantly reduced both in basal conditions and following an i.v. taurocholate infusion (0.5 mumol/min/100 g body wt). Biliary glutathione secretion was also significantly decreased following exercise. Cholestasis was caused by an impairment of both bile acid-dependent (BADF) and bile acid-independent fraction (BAIF) of bile flow (-25% and -29% respectively). Exercise caused a delay in the peak appearance time and a reduced biliary secretion of horseradish peroxidase, suggesting alterations in the functional integrity of the cytoskeleton. To test the protective effects of S-adenosyl-L-methionine (SAMe), rats received the drug for ten days at a daily dose of 8 mg/kg i.p. SAMe administration prevented hepatic glutathione depletion due to exercise, normalizing both bile flow and bile acid as well as glutathione secretion. Our results suggest that both glutathione depletion and alterations in fluidity and composition of hepatocyte membranes could contribute to the development of exercise-induced cholestasis.
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PMID:Impairment of bile secretion induced by exhaustive exercise in the rat. Protective effects of S-adenosyl-L-methionine. 832 15

It is well known that physical training permits an animal to respond successfully to exercise loads of various types, intensities, and durations. Furthermore, the trained animal can sustain the activity for a long period before the fatigue becomes limiting. The effects of physical training on the antioxidant defenses of tissues and on their susceptibility to damage induced by exhaustive exercise have been investigated. Therefore, untrained rats were sacrificed either at rest or immediately after swimming to exhaustion. Rats trained to swim for 10 weeks were also sacrificed, 48 hr after the last exercise, either at rest or after exhaustive swimming. Homogenates of liver, heart, and muscle were used for biochemical determinations. Mitochondrial and sarcoplasmic (SR) or endoplasmic (ER) reticulum integrity was assessed with measurements of respiratory control index and latency of alkaline phosphatase activity. Lipid peroxidation was measured by determination of malondialdehyde and hydroperoxides. Additionally, the effect of training on the antioxidant protection systems of tissues was examined by determining the glutathione peroxidase and glutathione reductase activity and the overall antioxidant capacity. Mitochondrial, SR, and ER integrity and lipid peroxidation were similar in trained and untrained at rest animals, whereas the glutathione peroxidase and glutathione reductase activity and the overall antioxidant capacity of tissues were greater in trained animals. The exhaustive exercise gave rise to tissue damage irrespective of the trained state, as documented by similar loss of SR and ER integrity, and by increase in lipid peroxidation found in exhausted trained and untrained rats. Because exercise endurance capacity was greatly increased by training, our results suggest that free radical-induced damage in muscle could be one of the factors terminating muscle effort. In effect, the greater antioxidant level should allow trained muscle to withstand oxidative processes more effectively, thus lengthening the time required so that the cell function is sufficiently damaged as to make further exercise impossible.
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PMID:Antioxidants, tissue damage, and endurance in trained and untrained young male rats. 866 Jun 84

We studied the effects of physical training on antioxidant defences and susceptibility to damage induced by exhaustive exercise in tissues of adult (12 mo) rats. Therefore, untrained animals were sacrificed either at rest (n = 8) or immediately after swimming to exhaustion (n = 8). Rats trained to swim for 10 weeks were also sacrificed, 48 hr after the last exercise, either at rest (n = 8) or after exhaustive swimming (n = 8). Integrity of mitochondria and sarcoplasmic (SR) or endoplasmic (ER) reticulum of liver, heart, and muscle was assessed by measuring mitochondrial respiratory control and latency of alkaline phosphatase activity. Lipid peroxidation was measured by determination of malondialdehyde and hydroperoxides. Additionally, the effect of training on tissue antioxidant systems was examined by determining the glutathione peroxidase (GPX) and glutathione reductase (GR) activity and the overall antioxidant capacity (CA). Membrane integrity was unaffected by training in liver and muscle, and improved in heart of at rest animals, whereas lipid peroxidation was reduced in both liver and heart. Glutathione peroxidase and glutathione reductase activity, and overall antioxidant capacity were increased (p < 0.05) by training in liver and muscle. In heart, antioxidant capacity was increased from 0.21+/-0.01 to 0.33+/-0.02 (p<0.05), but glutathione peroxidase activity remained unchanged (p>0.05), and glutathione reductase activity was decreased from 3.56+/-0.08 to 2.27+/-0.10 micromol x min(-1) x g(-1) (p < 0.05). The exhaustive exercise gave rise to tissue damage irrespective of trained state, as documented by similar loss of SR and ER integrity, and increase (p<0.05) in lipid peroxidation found in exhausted trained and untrained rats. However, the above changes were elicited by exercise of greater duration in trained than in untrained rats (340+/-17 min and 233+/-6 min, respectively). These findings support the view that free radical-induced damage in muscle could be one of the factors involved in muscle fatigue. If so, the increased endurance in trained rats should reflect lengthening of the time required for the oxidative processes to sufficiently impair cell functions so as to make further exercise impossible.
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PMID:Effect of training on antioxidant capacity, tissue damage, and endurance of adult male rats. 941 71


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