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)

Influence of alimentary zinc deficiency on nitrogen elimination and activities of urea cycle enzymes This study was conducted to investigate whether the hyperammonaemia shown in earlier zinc-deficiency experiments was the result of disturbed enzyme activities of the urea cycle. For this study 36 male Sprague-Dawley rats with an average body weight of 85 g were divided into three experimental groups of 12 animals each. Group 1 received the semisynthetic zinc-deficient diet (AIN-93G; 1.2 mg Zn/kg DM) ad libitum over 33 experimental days. Group 2 received the zinc-sulphate-supplemented control diet (60 mg Zn/kg DM) ad libitum and group 3 received the same diet matched to the feed intake of the zinc-deficient rats. Alimentary zinc deficiency reduced the zinc concentration and the activity of the alkaline phosphatase in serum by 75 and 67%, respectively. The activity of the glutamate dehydrogenase and the concentrations of ammonia and urea in the serum of the zinc-deficient rats showed no significant differences compared with pair-fed control rats. On the other hand the hepatic activity of the mitochondrial localized glutamate dehydrogenase of the zinc-deficient rats was significantly increased and the carbamoylphosphate synthetase and ornithine carbamoyltransferase were reduced about half in comparison with both control groups. The activities of the cytosolic liver enzymes such as argininosuccinate synthetase, argininosuccinase and arginase were again significantly increased in zinc-deficient rats compared with both control groups. The increased hepatic activity of the glutamate dehydrogenase possibly led to an enhanced NH(3) elimination in addition to urea synthesis. The typical reduction of feed intake in consequence of zinc deficiency is therefore not the cause of hyperammonaemia due to disturbed urea synthesis, as has been hypothesized in earlier studies.
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PMID:[Influence of alimentary zinc deficiency on nitrogen elimination and enzyme activities of the urea cycle]. 1168 72

The aim of this investigation was to determine if the hyperammonaemia shown in previous zinc-deficiency experiments was the result of disturbed enzyme activities for urea synthesis caused by zinc deficiency per se or was a secondary effect of the reduced feed intake accompanying energy and protein deficiency. For this, 24 male Sprague-Dawley rats with an average body weight of 109 g were divided into two groups of 12 animals each. Both groups were force fed by intragastric tube four times daily over 11 experimental days. Group 1 received a zinc-deficient diet (1.3 mg Zn/kg diet) in a total amount of 11.6 g/day/animal. Group 2 received the zinc sulphate-supplemented control diet (25 mg Zn/kg diet) in the same amount. This technique made it possible to supply even the zinc-deficient rats with sufficient nutrients over the whole experimental period in the same manner as for the control rats, at the same time and with the same dietary amounts. At the end of the experiment, the serum zinc concentration and the alkaline phosphatase activity were significantly reduced in the zinc-deficient rats by 59 and 37%, respectively, in comparison with control animals. This showed a severe alimentary zinc-deficiency status of the animals. The concentrations of ammonia and urea, as well as the activity of glutamate dehydrogenase in serum, were not influenced by the zinc-deficient nutrition within the experimental time. Likewise, the mitochondrial activities of glutamate dehydrogenase and carbamoylphosphate synthetase in the liver were not affected by the alimentary zinc concentration. On the contrary, the activities of ornithine carbamoyltransferase and cytosolic liver enzymes argininosuccinate synthetase, argininosuccinase and arginase were significantly increased in comparison with control rats. In the case of a sufficient supply of nutrients, alimentary zinc deficiency did not cause hyperammonaemia owing to disturbed urea synthesis, as previously hypothesized.
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PMID:[Nitrogen detoxification in artificially-fed zinc-deficient rats]. 1168 84

Birds have evolved alternate physiologic strategies to contend with dehydration, starvation, malnutrition, and reproduction. Basic anatomic and functional differences between birds and mammals impact clinical chemistry values and their evaluation. Interpretation of the results of standard biochemical analyses, including BUN, alanine aminotransferase, aspartate aminotransferase, creatine kinase, gamma glutamyltransferase, bilirubin, ammonia, alkaline phosphatase, cholesterol, bile acids, glucose, albumin, globulins, calcium, phosphorus, prealbumin (transthyretin), fibrinogen, iron, and ferritin, is reviewed and discussed in relation to these physiological differences. The use and interpretation of alternative analytes appropriate for avian species, such as uric acid, biliverdin, glutamate dehydrogenase, and galactose clearance, also are reviewed. Normal avian urine and appropriate use of urinalysis, an integral part of laboratory diagnosis in mammalian species that frequently is omitted from avian diagnostic protocols, is discussed.
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PMID:Clinical chemistry of companion avian species: a review. 1218 2

Hepatic encephalopathy and elevated serum ammonia levels occur commonly after portacaval shunt and are hypothesized to be, in part, due to decreased hepatic blood flow. Prior work has demonstrated increased blood flow to the liver following hepatic periarterial neurectomy. In this experimental study, we investigated the functional, hemodynamic, and histopathological changes in the liver and kidney occurring after the addition of hepatic periarterial neurectomy to side-to-side portacaval shunt in dogs. It is our hypothesis that the addition of hepatic periarterial neurectomy to portacaval shunt will decrease postshunt ammonia levels. Side-to-side portacaval shunt was performed in 12 dogs (group I). Hepatic periarterial neurectomy was added to portacaval shunt in 9 dogs (group II). Serum levels of ammonia, urea, creatinine, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, albumin, and bilirubin together with hepatic blood flow were determined in both groups preoperatively and on postoperative day 21. The pre- and postoperative histopathologic changes of the liver and kidney were evaluated. There was significantly less postoperative elevation of serum ammonia and aspartate aminotransferase when hepatic periarterial neurectomy was added to the portacaval shunt procedure. Hemodynamic studies of hepatic artery and hepatic tissue indicated better blood flow in group II. The histopathologic evaluation of group II showed expansion of sinusoids, portal vessels, and portal areas and increased portal fibrosis as compared to group I. The results of this experimental study show that adding hepatic periarterial neurectomy to the portacaval shunt procedure improves postoperative serum levels of ammonia and aspartate aminotransferase and hepatic artery and tissue blood flow.
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PMID:An attempt to decrease ammonia levels after portacaval anastomosis in dogs: hepatic periarterial neurectomy. 1235 34

A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen. On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. Urinalysis revealed an elevated specific gravity and numerous muddy granular casts. Hepatitis A, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. 1258 38

The aim of this study was to evaluate a novel bioartificial system in a canine model of acute liver failure. An acute liver failure model in canines was induced by an end-side portocaval shunt combined with common bile duct ligation and transection. The bioartificial liver system, which utilized blood perfusion through a hollow fiber bioreactor from BIOLIV A3A inoculated with 1.0 - 3.1 x 1010 porcine hepatocyte spheroids, was developed for the treatment of acute liver failure. Sixteen acute liver failure model canines were divided between a group treated with bioartificial liver (n=8) and a control group (n=8) for 5 h. Blood alanine aminotransferase (ALT), alkaline phosphatase (AKP), total bilirubin (TBi), direct bilirubin (DBi), prothrombin time (PT), ammonia levels, and the ratio of branched chain to aromatic amino acids (Fischer's ratio) were determined. ALT, AKP, TBi, DBi, and ammonia levels were significantly elevated, PT was significantly prolonged, and Fischer's ratio decreased significantly in the canine model of the two groups on day 14 after operation compared to baseline. There were no significant differences between the two groups in laboratory data before treatment. In canines treated with the bioartificial liver system, ALT, AKP, TBi, DBi, and ammonia levels decreased significantly, PT was significantly shortened, Fischer's ratio was significantly elevated after treatment, and the survival rate by day 7 after treatment was 100%. In canines in the control group, on the other hand, there were no significant differences in ALT, AKP, TBi, DBi, PT, and ammonia levels between pretreatment and posttreatment, though these indices decreased to a slight degree after treatment. The survival rate by day 7 after treatment was 62.5% in the control group. Fischer's ratio decreased after treatment. ALT, AKP, TBi, DBi, PT, and ammonia levels in the bioartificial liver system group were lower, and Fischer's ratio and survival rate were higher than those in the control group after treatment. These results indicate that the novel bioartificial liver system we developed has a significant impact on the course of canine acute liver failure model and has potential advantages for clinical use in patients with acute liver failure.
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PMID:Bioartificial liver inoculated with porcine hepatocyte spheroids for treatment of canine acute liver failure model. 1282 16

The overexpression of p27, a cyclin-dependent kinase (CDK) inhibitor, has been shown to effectively inhibit cell growth at the G1-phase of different cell lines, potentiating a valid genetic strategy for cell proliferation control. In order to characterize the energy requirements after p27 overexpression in CHO cells expressing SEAP (secreted form of the human alkaline phosphatase enzyme), key metabolic parameters were evaluated. Cell growth inhibition led to a significant increase in cell size concomitant with a 2-fold increase in cell protein content. The simultaneous increase of the intracellular proteolytic activity with protein content suggests higher protein synthesis. A general 2-fold increase in oxygen, glutamine and glucose consumption rates, coupled with an increase in lactate and ammonia production was observed. p27 overexpression led to a significant increase in the intracellular pool of AMP (8.5-fold), ADP (6-fold) and, more uncommonly, ATP (4.5-fold). Nevertheless, cells were able to maintain the equilibrium among the three adenine nucleotides since both the ATP/ADP ratio and the energy charge values remained similar to those observed with non-growth inhibited cells. This work shows that the observed 4-fold increase in SEAP specific productivity after cell growth inhibition by p27, occurred concomitantly with a higher expenditure of cell energy. This characterization of cell metabolism becomes important in demonstrating the applicability of growth inhibition systems.
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PMID:Metabolic changes during cell growth inhibition by p27 overexpression. 1285 62

Trimethoprim-sulfamethoxazole (TMP-SMZ) is one of the most commonly used antibiotics. Although many of its adverse effects are well recognized, TMP-SMZ related hepatotoxicity is considered rare and is usually characterized by cholestasis or mixed hepatocellular-holestatic reactions. In this study, we describe the case of a previously healthy young man with acute fulminant liver failure caused by TMP-SMZ. The patient presented with complaints of 'flu-like' symptoms with myalgia and fever after taking TMP-SMZ for 7 d for otitis externa. The patient subsequently developed fever, worsening jaundice, and a rash on his neck and chest. Liver enzymes peaked on day 3 with alanine aminotransferase (ALT) 11,549, aspartate aminotransferase (AST) 23,289, alkaline phosphatase 245, and total bilirubin 10.3 mg/dL, with a conjugated bilirubin of 8.3 mg/dL, prothrombin time (PT) 60.5 s, partial normalized ratio (PTT) 49 s, and international normalized ratio (INR) 7.5. Of note, acetaminophen level on admission was undetectable. Serology for hepatitis A, B, C, cytomegalovirus, HIV, toxoplasmosis, and blood cultures were all negative. The patient developed hepatic encephalopathy with hallucination on day 4. Laboratory tests revealed a serum ammonia level of 190 U, serum creatinine kinase (CK) 10,466 (42 on admission), serum creatinine 8.2 mg/dL (1.2 on admission), and significant metabolic acidosis. Renal ultrasound was unremarkable. The patient was started on hemodialysis for acute renal failure. Meanwhile, liver transplantation assessment was also initiated. On day 8 post-admission (15 d after taking TMP-SMZ), the patient received a successful orthotopic liver transplant.
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PMID:Successful orthotopic liver transplantation after trimethoprim-sulfamethoxazole associated fulminant liver failure. 1470 31

The molecular adsorbent recirculating system (MARS) method removes from the blood catabolites either free in the plasma water such as uremic toxins and ammonia, taking advantage of dialysis or free albumin bound ones, like hepatic toxins, transferring them from the albumin in the blood to the albumin circulating in a closed loop where toxins are removed by adsorbtion on resins (charcoal and ion exchange resin). The efficacy of the method in removing the hepatic toxins either in the acute or in the acute on chronic liver failure is demonstrated in numerous studies. Based on these findings, 10 patients affected by acute on chronic liver failure were treated. The results demonstrated that the method, powerfully removing ammonia, bilirubin and bile acids (taken as method efficacy markers), reduced the blood concentrations of these molecules remarkably; allowing the elimination of the refractory pruritus (due to the lowering of plasma bile acid levels), an almost constant symptom in chronic liver diseases, especially with cholestasis, and improves other parameters (cholinesterase, alkaline phosphatase and prothrombin activity). These results agree with those reported in the literature concerning the efficacy of MARS in the replacement of the liver detoxifying function.
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PMID:[Molecular Adsorbent Recirculating System in liver function replacement therapy]. 1578 94

Twenty-four growing male buffalo calves (one year of age; 88.54 +/- 3.81 kg average body weight) were divided into three comparable groups (I, II and III) on the basis of their body weight (BW) in a completely randomised design to study the effect of long term feeding of ammoniated wheat straw (AWS) and hydrochloric acid treated ammoniated wheat straw (HCl-AWS) on blood biochemical changes. The animals were offered a concentrate mixture (CM) along with wheat straw (WS), ammoniated wheat straw (AWS) (4% urea at a 50% moisture level) and hydrochloric acid treated ammoniated wheat straw (HCI-AWS) (4% urea at a 50% moisture level and HCI added to trap 30% of NH3 evolved) in groups I, II and III, respectively for an average daily gain (ADG) of 500 g. All the diets were made iso-nitrogenous by preparing three types of concentrate mixtures of different CP levels. The blood was collected from the jugular vein randomly from three animals of each group initially after 8 months post feeding and subsequently after two months interval up to 14 months of experimental feeding. Due to urea ammoniation, the CP content of WS increased from 3.66 to 8.51 and was further increased to 11.35 due to the addition of HCl during urea-ammoniation of wheat straw. The cumulative period mean plasma glucose values (mg %), in group II (53.13) were significantly (P < 0.001) higher than those in groups I (48.44) and III (50.60). The cumulative period mean values of serum albumin and globulin (g %) were not significantly different and were comparable among the groups I (3.33 and 3.06), II (3.53 and 2.97) and III (3.49 and 2.94). The cumulative period mean values of serum albumin: globulin ratio and total protein values were not significantly different among the different groups. Serum urea and creatinine values were significantly (P < 0.001) higher in group III (58.66 and 2.24) as compared to groups I and II. The cumulative period mean values of serum alkaline phosphatase (ALP) (KA units) did not differ significantly, but serum glutamate pyruvate transaminase (SGPT) and glutamate oxaloacetate transaminase (SGOT) values (units x mL(-1) were significantly (P < 0.001) higher in groups II and III than in group I. The cumulative period mean values of T3 (ng x mL(-1)) did not differ significantly among the groups, but T4 values were significantly (P < 0.001) higher in group III (22.74) than in groups 1 (21.41) and II (20.89), respectively. Since the mean values of all the blood parameters were within the normal range, it may be concluded that feeding of ammoniated wheat straw treated with and without HCl to growing male buffalo calves for fourteen months has no adverse effect on the blood biochemical parameters.
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PMID:Effect of long term feeding of ammoniated wheat straw treated with or without HCl on blood biochemical parameters in growing male buffalo (Bubalus bubalis) calves. 1595 22


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