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)

Venous blood values were determined on 19 Southdown sheep (9 adult ewes and 10 wether lambs). Principal sheep were given 12.5 ml of 3.3M urea solution/kg of body weight, which produced acute ammonia toxicosis. Whole blood ammonium-nitrogen was determined by ion exchange; venous blood gases and pH were measured with a pH blood gas analyzer; and 23 serum chemical analyses were obtained with a sequential multiple autoanalyzer computer. Analysis of variance for the data revealed significant changes for 20 values. The values are presented and discussed with regard to those that changed beyond acceptable limits (whole blood ammonium-nitrogen, venous blood pH, serum glucose, serum lactate dehydrogenase, serum alkaline phosphatase, serum creatine kinase, serum urea nitrogen, serum inorganic phosphorus, serum sodium, and serum potassium), those that changed within acceptable limits (PVo2, PVco2, serum triglycerides, serum free fatty acids, plasma volatile fatty acids, serum aspartate aminotransferase, serum total protein, serum albumin, serum creatinine, urea nitrogen-creatinine ratio, serum uric acid, serum cholesterol, serum low-density lipoproteins, serum calcium, serum iron and serum chloride), and those with no change (total and direct serum bilirubin and albumin-globulin ratio). Metabolic consequences of ammonia toxicosis are considered with regard to energy, lipid , protein, and acid-base and electrolyte balances. Blood values having possible laboratory diagnosis value and considerations for therapeutic adjustment are discussed.
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PMID:Ovine blood chemistry values measured during ammonia toxicosis. 710 77

Three young dogs with a history of apathy, anorexia and weight loss were presented with severe ascites. Abnormal laboratory findings include hypoalbuminaemia and increased activities of alkaline phosphatase, serum aspartate amino-transferase, serum glutamic pyruvic transaminase and gamma-glutamyl transferase. Ammonia tolerance was also abnormal. At autopsy ascites and peripheral portosystemic collaterals were found. The livers were abnormally small and firm and their surfaces were irregular. Histologically, there was marked periportal fibrosis, increased numbers of bile ductules and arteriolae in the portal areas and an absence of normal portal vein tributaries. No inflammatory changes were found. These lesions are discussed in relation to the various causes of hepatic fibrosis.
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PMID:Hepatoportal fibrosis in three young dogs. 711 76

Biochemical changes in the air-breathing catfish, Clarias batrachus (Linn.) exposed to a sublethal level of carbofuran (2,3-dihydro-2,2-dimethyl-7-benzofuranyl methylcarbamate) at 0.5 ppm concentration in ambient water for a period of 30 days were assessed. A small reduction in growth rate was observed in the fish treated with 0.5 ppm carbofuran for 60 days although no mortality or any apparent symptom of toxicity could be noted. Studies were carried out on the activities of certain enzymes of intermediary metabolism viz., glucose 6-phosphatase, alkaline phosphatase, acid phosphatase, Na+, K+-ATPase, GOT and GPT in certain vital tissues of the fish exposed to carbofuran (0.5 ppm) for 30 days. Exposure to carbofuran resulted in sharp inhibition of acetylcholinesterase activity in brain of the fish which recovered rather rapidly after terminating pesticide treatment and maintaining the fish in clean freshwater. Ratio of the levels of calcium/phosphorus in serum showed significant diminution in experimental groups of fish compared to controls. Level of ammonia in serum of experimental fish was markedly increased while excretion of ammonia by fish showed concomitant decrease. The bioaccumulation level of the pesticide and its degraded product, 3-hydroxy-carbofuran in liver tissue was measured by gas chromatography. A rationale of the effect of carbofuran on metabolism vis-a-vis toxicity in the fish has been suggested.
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PMID:Certain biochemical responses in the air-breathing catfish Clarias batrachus exposed to sublethal carbofuran. 712 66

The effect of arterialization of the portal vein was investigated in cirrhotic dogs with a portacaval shunt. In dogs receiving a portacaval shunt only (PCS), the pressure in the intrahepatic portal vein fell to about 10% of the preshunt value, while the total hepatic blood flow was reduced by 63.9%. By contrast, in dogs with arterialization in addition to a portacaval shunt (PCS + A), the pressure in the portal vein was almost restored to preshunt levels, and the decrease in total hepatic blood flow was only 35.7%; this difference in the reduction of hepatic perfusion is significant (p less than 0.01). 2 weeks after the operation, PCS + A dogs had lower plasma levels of bilirubin and alkaline phosphatase, and a higher antipyrine clearance than PCS dogs (p less than 0.05). This improvement, however, was of short duration. The results of the ammonia tolerance test were not affected by the arterialization procedure.
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PMID:Temporary beneficial effect of arterialization of the liver in cirrhotic dogs with a portacaval shunt. A preliminary report. 712 51

The numerous physiological and nutritional factors which influence the concentration of serum calcium are considered. The causes of hypercalcaemia and hypocalcaemia are briefly discussed, with particular reference to the clinical symptoms and pathology. The effect of the acid-base status on the serum-ionized calcium level is stressed. The causes of changes in the serum concentrations of phosphorus and magnesium are briefly reviewed, along with the abnormalities of lactate, pyruvate, and hydrogen ion concentrations. The kidney function tests, blood urea nitrogen, serum creatinine, and the renal clearance tests are discussed, with emphasis placed on correlating their results with the findings from repeated urinalyses. The important physiologic influences and pathological processes which result in changes in the concentrations of these parameters are delineated. The causes of increases in the serum enzymes, alkaline phosphatase, alanine transaminase, asparate transaminase, lactic dehydrogenase, sorbitol dehydrogenase, glutamic dehydrogenase, gamma glutamyl transpeptidase, creatinine phosphokinase, amylase and lipase are discussed. The changes in serum bilirubin concentration and its components are fully described, with emphasis placed on the correlation of the findings with urinalysis data and the complexities resulting from the numerous pathologic conditions causing jaundice. These conditions are listed for each of the domestic animals. The other liver function tests, bromosulphthalein dye retention or excretion, serum uric acid and blood ammonia concentration are briefly considered. All the tests described are very useful, and frequently essential, in aiding the veterinary practitioner to arrive at a diagnosis and prognosis, but they never replace clinical acumen.
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PMID:Correlation of changes in blood chemistry with pathological changes in the animal's body: II Electrolytes, kidney function tests, serum enzymes, and liver function tests. 727 79

In this paper clinical similarities between sickle cell anemia patients and zinc deficient subjects, the latter as reported from the Middle East have been presented. Zinc levels in plasma, red cells, hair and neutrophils were decreased in our adult patients with SCA. The activities of certain zinc dependent enzymes such as plasma RNase, red cell carbonic anhydrase, leucocyte alkaline phosphatase, and deoxythymidine kinase activity in freshly synthesized collagen connective tissue were consistent with the concept that indeed zinc deficiency occurred in SCA patients. Zinc supplementation under controlled conditions showed that the SCA patients gained weight, their serum testosterone level increased and plasma ammonia level decreased. Finally, we also observed abnormal dark adaptation in some SCA patients which improved following zinc supplementation. Inasmuch as we have previously reported that the number of irreversible sickle cells decrease following zinc supplementation, we would like to suggest that zinc supplementation at earlier age may be benefical in preventing organ damage. In conclusion, zinc supplementation should be prescribed for patients with SCA, particularly if they show evidences for zinc deficiency.
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PMID:Zinc deficiency and effects of zinc supplementation on sickle cell anemia subjects. 729 Dec 6

Studied were 12 cows with protracted, recurrent acidosis of the rumen, 4 cows with alkalosis, and 2 calves with experimental acidosis, following up the changes in the rumen content and their impact on the liver. The diseased animals were investigated both clinically and by laboratory tests with regard to alkaline phosphatase, plasma cholinesterase, SGOT, SGPT, alkali reserves, bilirubin, blood sugar, protein function of the liver (flocculation tests), biopsy of the liver, urine pH, urobilinogen, sedimentation test and ketone bodies, rumen pH, rumen infusoria, glucose-fermenting and cellulose-digesting activity, breakdown of nitrates, butyric acid, and ammonia gas. It was found that recurrent physiologic deviations of the rumen content play an essential pathogenetic role in liver injury. The more substantial and continuous the deviations the more severe the liver diseases. Studies revealed that along with other factors the recurrent acidosis and alkalosis of the rumen content could be claimed to be an immediate cause of the liver diseases in high producing cows. Histologically, the liver of cows with slightly expressed acidosis of the rumen showed granular degeneration, and of cows with protracted acidosis--fatty degeneration, activation of the reticulo-endothelial system, and leukocytes in the capillar sinusoids. Liver biopsy in the case of experimental acidosis demonstrated also decrease in the glycogen content of the hepatocytes.
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PMID:[Liver diseases and their relationship to forestomach function in highly productive cows]. 734 34

Substrates commonly used for localizing bone Golgi apparatus (GA) acid phosphatase (AcPase), e.g., beta-glycerophosphate, p-nitrophenylphosphate, cytidine-5'-monophosphate, and di(dicyclohexylammonium)-2-napthylthiolphosphate, give strong staining not only of GA but also of lysosomes. Thiamine pyrophosphate and inosine-5'-monophosphate--substrates that give good GA staining in some soft tissues--give only lysosomal staining in bone. No previously used substrate or substrate-effector combination has selectively localized the GA acid phosphatase in bone. This article describes results using a new AcPase medium having pyridoxal-5'-phosphate (PLP) as substrate. In bone this medium produced strong staining of the osteoblast GA, but relatively little staining of lysosomes, including lysosomes in osteoclasts. The weak lysosomal staining was almost totally eliminated, without affecting the GA reaction, by pretreating the tissue in 0.3% NH3 solution. Conversely, elevated ionic strength of the substrate medium eliminated the GA reaction, while having little effect on lysosomal staining. The GA enzyme was very sensitive to 1 mM tartrate whereas the lysosomal enzyme was not. These differences suggest the presence of distinct isoenzymes in the two locations. The distribution of osteoblasts with stained GA coincided with the distribution of strongest alkaline phosphatase activity and rapid bone mineralization, supporting previous suggestions that osteoblast GA AcPase is involved in the processing of one or more newly synthesized bone matrix components.
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PMID:Selective localization of a Golgi apparatus acid phosphatase isoenzyme in bone using pyridoxal-5'-phosphate. 735 10

Changes in oxidative metabolism were studied in hepatopancreas, muscle, and hemolymph of the edible crab Scylla serrata, exposed to a sublethal concentration (2.5 ppm) of cadmium chloride. A significant decrease in glycogen, total carbohydrates, and pyruvate and an increase in lactate levels in hepatopancreas and muscle were observed. Hemolymph sugar levels were increased in experimental crabs. An increase in phosphorylase suggested increased glycogenolysis during cadmium toxicity. The decrease in lactate dehydrogenase activity and the increase in lactate content indicated reduced mobilization of pyruvate into the citric acid cycle. Krebs cycle enzymes such as succinate dehydrogenase and malate dehydrogenase were found to be decreased, suggesting impairment of mitochondrial oxidative metabolism as a consequence of cadmium toxicity. Glucose-6-phosphate dehydrogenase activity was increased, suggesting enhanced oxidation of glucose by the HMP pathway. Cytochrome-c oxidase and Mg2+ ATPase activity levels decreased, indicating impaired energy synthesis during cadmium stress. Acid and alkaline phosphatase activities increased, suggesting enhanced breakdown of phosphates to release energy in view of impaired ATPase system during cadmium exposure. A significant decrease in protein and free amino acid and an increase in ammonia, urea, and glutamine levels were observed in the tissues during exposure. An increase in protease, alanine aminotransaminase, and aspartate aminotransaminase suggested increased proteolysis and transamination of amino acids. The increase in glutamate dehydrogenase, AMP deaminase, and adenosine deaminase indicated increased ammonia production. The increased arginase and glutamine synthetase suggested the detoxification or mobilization of ammonia toward the production of urea and glutamine. These results suggest that cadmium affects oxidative metabolism and induces hyperammonemia, and crabs switch over their metabolic profiles toward compensatory mechanisms for the survivability in cadmium-polluted habitats.
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PMID:Changes in oxidative metabolism in selected tissues of the crab (Scylla serrata) in response to cadmium toxicity. 753 86

The present study was performed to measure the uptake of main renal cortical fuel substrates (glutamine and lactate) and the release of the main renal cortical products (ammonia and glucose) by cortical slices from gentamicin-treated rats. Experiments were done in 2 groups of female Wistar rats (250 g): In gentamicin group (n = 13), rats were injected s.c. with gentamicin-sulphate 100 mg/Kg body wt/day for 5 days. Control rats (n = 13) received isotonic saline. After anesthesia and blood sampling, renal cortical slices were obtained and incubated with L-glutamine and/or lactate at 1 or 5 mM concentration, containing L-glutamate and/or pyruvate at 0.1 or 0.5 mM. Creatinine clearance was reduced to a 50% in gentamicin-treated rats. In addition these animals showed a sharp increase in urinary excretion of N-acetyl-beta-D-glucosaminidase and alkaline phosphatase. Light microscopy examination revealed extensive cell necrosis and tubular obstruction of the proximal tubules in kidneys of rats injected with gentamicin. The renal cortical gentamicin concentration of rats injected with gentamicin was 310 +/- 43 mu/g, whereas it was undetectable in control rats. Cortical slices from gentamicin-treated rats, compared to control ones, showed a reduced production of ammonia and glucose, without differences in glutamine or lactate extraction. These alterations can be explained by both the increased rate of anabolic reactions to recover cell damage associated to renal failure, as well as by a direct effect of gentamicin on the rate of carboxylation reactions.
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PMID:Effect of gentamicin treatment on glutamine and lactate metabolism by the renal cortex of the rat. 769 Dec 12


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