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)

During a long-term study in the rat some enzyme activities were determined in plasma, lung, spleen and skeletal muscle. Twelve rats of each sex were investigated every 49 days from 35 until 1115 days of life. Lactate dehydrogenase in lung and spleen decreases; in muscle and plasma, however, the activity varies considerably. Malate dehydrogenase in the tissues remains nearly unchanged apart from distinct peaks in the first year of life; in plasma the activity takes an M-shaped course. In contrast to the changes of glutamate dehydrogenase in the tissues with a tendency to diminish, this enzyme increases in plasma during the lifetime. Aspartate aminotransferase activity in the tissues, except muscle, varies with a rhythmical behaviour, and in plasma shows a gradual increase. Alanine aminotransferase in lung and spleen has two activity peaks. In muscle this enzyme varies only slightly after a steep initial decrease. In plasma the activity has a tendency to rise. Creatine kinase in the tissues reveals several activity peaks. In plasma the activity course is U-shaped. Adenylate kinase in spleen and lung rises, whereas in muscle the activity varies considerably. The nearly identical decrease of alkaline phosphatase activity in the tissues during ageing is also reflected by a concomitant behaviour in plasma. Leucine arylamidase in lung and muscle both have a U-shaped characteristic, whereas in spleen the activity changes in a shorter period. In plasma, a rhythmical behaviour is apparent. Aldolase in plasma tripled during the observation period. Except for lactate dehydrogenase and aldolase, distinct sex-differences are observed in plasma. With progressive age the animals suffer increasingly from characteristic diseases, which beside experimental components have influenced the enzyme pattern. Enzyme activities in plasma and tissues show a complex pattern and are only of limited importance in understanding the ageing process.
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PMID:Long-term observation of plasma and tissue enzyme activities in the rat. 720 25

5-Aminosalicylic acid-O-sulfate (5-ASA sulfate), a new agent for the treatment of ulcerative colitis and Crohn's disease of the large intestine, was investigated for its pharmacokinetic and toxicological properties, following local and systemic application. 5-ASA sulfate can be considered as a non-toxic agent after single oral intake in rats (14-day LD50 > 6000 mg/kg b.w.). Oral application of 2500 mg 5-ASA sulfate/kg b.w./d for 28 days to rats resulted in significantly increased body weight gain and food and water consumption. Alanine aminotransferase and alkaline phosphatase values were elevated in high-dosed (2500 mg/kg b.w./d p.o.) males. Relative liver weights were significantly increased in high-dosed males and females and the macroscopical inspection revealed thickened liver margins. The no-effect level following 28 days of oral application to rats was determined as 500 mg 5-ASA sulfate/kg b.w./d. In acute local tolerance studies in rabbits, 5-ASA sulfate is rated as non-irritant to the skin and the eye. After a single oral administration of 1800 mg 5-ASA sulfate to 5 healthy human test subjects, 5-ASA sulfate was almost completely metabolized by all test subjects within 3 days; mean urinary and faecal excretion of unchanged 5-ASA sulfate amounted to only 6.7% of the administered dose. A high faecal excretion of the active metabolite 5-aminosalicylic acid (5-ASA) (21.2% of the administered dose) and a low urinary excretion (1.4% of the administered dose) were observed.
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PMID:Experimental studies on the pharmacokinetics and toxicity of 5-aminosalicylic acid-O-sulfate following local and systemic application. 774 89

A crude, whole-body extract of female or male heartworms was injected IV into 28 dogs with and 22 dogs without heartworm (HW) infection. The female HW extract caused shock in 22 of 24 dogs with and 12 of 20 dogs without HW infection. The male HW extract induced shock in 4 of 4 dogs with and 1 of 2 dogs without HW infection. Prevalence of shock caused by female HW extract was significantly (P < 0.05) higher in dogs with than without HW infection; shock developed 5 to 30 minutes after HW injection. These signs were observed: marked decrease in blood pressure; collapse (initial collapse); paleness of mucous membranes; weak heart sounds; dyspnea; skin coldness; intestinal hyperperistalsis, and defecation; increases in RBC count, serum total protein concentration, serum osmolality, serum Na and blood glucose concentrations; and decreases in neutrophil, eosinophil, and platelet counts. Alanine transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased substantially from the time of initial collapse to 24 hours after HW injection. Of 39 dogs with shock, 29 recovered from initial collapse, but 5 of the 29 subsequently collapsed again (secondary collapse), with bloody diarrhea followed by death. Of these 39 dogs, 6 died during initial collapse without bloody diarrhea, and 4 were euthanatized during initial collapse. It was confirmed that HW extract had, in fact, induced shock. These clinical, hematologic, and biochemical findings were fundamentally similar to those associated with shock resulting from administration of drugs, such as diethylcarbamazine and milbemycin D, in microfilaremic dogs with HW infection.
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PMID:Clinical, hematologic, and biochemical findings in dogs after induction of shock by injection of heartworm extract. 787 76

Thirty children with sickle cell anaemia had their serum alanine aminotransferase, alkaline phosphatase, total protein, albumin and bilirubin, assayed during vaso-occlusive crisis and at recovery. Alanine aminotransferase, alkaline phosphatase and bilirubin levels were significantly higher during crisis than at recovery, (p < 0.005) especially in the young patient. However, the total protein and albumin levels were not significantly different in crisis and at recovery. A transient hepatic functional derangement during vaso-occlusive crisis is a probable explanation for the reported changes.
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PMID:Hepatic function tests in children with sickle cell anaemia during vaso occlusive crisis. 788 14

We have examined the effects of administration of the blood substitute, liposome-encapsulated haemoglobin (LEH), in the normovolaemic rat. Test groups included LEH, lyophilized EH, the liposome vehicle, unencapsulated haemoglobin and normal saline, which were injected into the tail vein (n = 6; n = 3 for sham and saline groups). Administration of LEH (2.5 g phospholipid, 1.25 g haemoglobin/kg rat) was followed by blood sampling at 2 h, 24 h, 1 wk and 2 wk. Blood samples were analysed for alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyltransferase, total and indirect bilirubin, serum creatinine, albumin, total protein, lipase, cholesterol, blood urea nitrogen, haematocrit, haemoglobin and differential white blood cell counts. Observed effects following injection were mild and transient, with baseline values recovered at 1 wk. Alanine aminotransferase increased moderately in the LEH group at 24 h to 601 +/- 143 IU/dl (P < 0.0001), with a return to baseline at 1 wk. Aspartate aminotransferase showed a smaller increase from 46 +/- 5 to 162 +/- 40 at 24 h and also returned to baseline at the 1 wk measurement (P < 0.001). The transient increase in serum transaminases was not observed for the lyophilized LEH group. Tissue sections showed accumulation of liposome groups in resident macrophages of the liver and spleen. Incubation of an adherent population of human peripheral blood monocytes with LEH in culture did not elicit the production of the inflammatory cytokine, tumour necrosis factor. Pre-incubation of monocytes with LEH prior to exposure to endotoxin did, however, result in a reduced expression of this inflammatory cytokine.
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PMID:Transient changes in the mononuclear phagocyte system following administration of the blood substitute liposome-encapsulated haemoglobin. 798 44

Blood alpha-fetoprotein, carcinoembyronic antigen, CA-19-9, alkaline phosphatase, gamma-glutamyltranspeptidase, alanine aminotransferase, aspartate aminotransferase, sorbitol dehydrogenase, glutamate dehydrogenase, hemoglobin and red cell sedimentation rate were measured in patients with stages III and IV gastric carcinoma and patients with benign diseases of the stomach. Alanine aminotransferase, sorbitol dehydrogenase and glutamate dehydrogenase were found diagnostically not informative in gastric carcinoma stages III and IV. A complex of measurements of alpha-fetoprotein, alkaline phosphatase, gamma-glutamyl transpeptidase and aspartate aminotransferase detected gastric carcinoma metastases to the liver in 84.6% of cases as against 61.5% detected by measurements of alpha-fetoprotein alone. A complex of measurements of carcinoembryonic antigen, CA-19-9, alkaline phosphatase, gamma-glutamyl transpeptidase, aspartate aminotransferase helped differentiate between gastric carcinoma stages III and IV. A complex of measurements of carcinoembryonic antigen, CA-19-9, alkaline phosphatase, gamma-glutamyl transpeptidase, aspartate aminotransferase, hemoglobin, and red cell sedimentation rate improved the diagnostic sensitivity in detection of gastric carcinoma stages III and IV to 70.8 and 100%, respectively.
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PMID:[Laboratory tests in the diagnosis of stomach cancer]. 800 Jul 94

Groups of rats were treated with graded doses of zineb or aldicarb solely or in association with copper sulphate for nine consecutive weeks. Body weight gain was retarded and thymus gland weight was decreased in all treated groups. A pronounced synergism between copper sulphate and zineb was noticed in lowering the weights of thymus, testes, and adrenal glands. Various degrees of reduction in hemoglobin concentration, red blood cells and platelet counts occurred after treatment with the above-mentioned agrochemical regimen. Copper sulphate synergised the elevation of serum alkaline phosphatase (AP) activity, and bilirubin concentration as well the reduction of hemoglobin concentration by zineb. Alanine aminotransferase (ALT) activity was significantly increased, while cholinesterase (ChE) activity was decreased in all treated groups. Serum triglycerides (TGs) were lowered in rats treated with medium or high doses of zineb or aldicarb.
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PMID:Toxic interactions between copper sulphate and some organic agrochemicals. 831 Apr 52

The objective of this study was to report the frequency of disulfiram-related elevations of four commonly used hepatic screening chemistries using a retrospective record review design. An inpatient alcoholism program was selected for the setting. Patients who had initial laboratory values within the normal range started daily supervised doses of disulfiram, then underwent follow-up testing after 2 and 4 weeks on the drug. The study population consisted of 108 patients receiving disulfiram and 27 patients who did not receive disulfiram (controls). The four screening serum chemistries performed were aspartate aminotransferase (SGOT), alanine aminotransferase (SGPT), alkaline phosphatase, and gamma-glutamyl transferase. Twenty-seven (25%) of the 108 patients who were taking 250 mg of disulfiram a day for 2 to 4 weeks had disulfiram-related elevations in alanine aminotransferase above the upper limit of normal, as opposed to one elevation in 27 patients (4%) for whom disulfiram was not prescribed. In the 108 patients (with initially normal serum chemistries) who were prescribed disulfiram, 32 were discontinued from the drug at 2 weeks and an additional 11 were discontinued from the drug at 4 weeks because of one or more abnormal serum chemistries. Alanine aminotransferase was the most specific and sensitive indicator of the four screening chemistries performed.
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PMID:Screening for disulfiram-induced liver test dysfunction in an inpatient alcoholism program. 838 24

The possibility that postmortem biochemical changes in blood might parallel drug redistribution and thus serve as markers was explored in a detailed case study. Eighteen blood and 14 tissue and fluid samples were taken at autopsy 16 h after the death of a 34-year-old female from amitriptyline overdose. Ranges of drug concentrations in blood were amitriptyline 1.8 to 20.2 micrograms/mL, nortriptyline 0.6 to 7.3 micrograms/mL, levels were lowest in femoral vein and highest in pulmonary vein blood. Corresponding levels of 17 amino acids showed markedly different patterns of site-to-site variability. There was a strong positive correlation between individual amino acid and drug concentrations in pulmonary blood samples (n = 5), particularly for glycine, leucine, methionine, serine, and valine. In blood samples from the great veins and right heart (n = 10), the correlation was less strong (r = 0.6 to 0.7). Methionine showed a strong positive correlation in pulmonary samples (r = 0.93), and negative correlation in great veing samples (r = -0.68). Lactic acid showed a strong negative correlation in pulmonary samples (r = -0.93) but a positive correlation in great vein samples (r = 0.71). Alanine aminotransferase, alkaline phosphatase, aspartate aminotransferase, gamma-glutamyl transferase, glucose, and bilirubin had a weak positive correlation with drug levels in great vein samples but not pulmonary samples. The results suggest that hepatic enzymes are relatively poor markers for postmortem hepatic drug shifts but that amino acids, particularly methionine, may be useful markers for pulmonary drug shifts.
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PMID:Possible markers for postmortem drug redistribution. 898 78

The objectives of this study were to 1) study the GH-insulin-like growth factor (IGF) axis in adult untreated Turner's syndrome compared to that in age-matched controls; 2) examine the effects of sex hormone substitution on this axis, 3) study the effects of route of administration of 17 beta-estradiol on the measured variables, and 4) examine the effects of sex steroids on hepatic function in Turner patients. Twenty-seven patients with Turner's syndrome were evaluated before and during sex hormone replacement, and an age-matched control group (n = 24) was evaluated once. Main outcome variables were GH and other measures of the GH-IGF axis, body composition, maximal oxygen uptake, sex hormone-binding globulin, and hepatic enzymes and proteins. The integrated 24-h GH concentration (IC-GH; micrograms per L/24 h) was reduced in women with Turner's syndrome (T) compared to controls [C; mean +/- SD, 18.3 +/- 12.0 (T) vs. 37.2 +/- 29.7 (C); P = 0.007]. However, multiple regression revealed that fat-free mass (FFM) and maximal oxygen uptake were significant explanatory variables (joint r = 0.77; P < 0.0005), accounting for 60% of the variance in the 24-h IC-GH. This association was also present in controls. After adjustment for these two variables, any difference in GH concentration between Turner patients and controls disappeared. Serum IGF-I and IGF-II were identical in Turner patients and controls despite the difference in 24-h IC-GH. The level of GH-binding protein (GHBP; nanomoles per L) was higher in Turner women [1.87 +/- 0.72 (T) vs. 1.22 +/- 0.33 (C); P = 0.0005]; after adjustment for FFM, the difference in GHBP levels disappeared between Turner patients and controls. During sex hormone treatment a significant increase was seen in the 24-h IC-GH (P = 0.02), FFM (percentage of weight; P < 0.0005) and maximal oxygen uptake (milliliters of O2 per kg/min; P = 0.02). Serum IGF-I was unchanged, whereas serum IGF-II (micrograms per L) decreased significantly [Turner, basal (TB), vs. Turner, treatment (TT), 860 +/- 135 vs. 823 +/- 150; P = 0.04]. Alanine aminotransferase (units per L), gamma-glutamyl transferase (units per L), and alkaline phosphatase (units per L) were significantly elevated during the basal study period, and all decreased during treatment [alanine amino-transferase, 55 +/- 55 (TB) vs. 30 +/- 20 (TT; P = 0.006); gamma-glutamyl transferase, 92 +/- 98 (TB) vs. 43 +/- 65 (TT; P = 0.003); alkaline phosphatase, 211 +/- 113 (TB) vs. 175 +/- 54 (TT); P = 0.06]. The route of administration of 17 beta-estradiol did not affect its actions. In conclusion, we found the GH-IGF axis in Turner's syndrome to be normal, with body composition and physical fitness exerting the same modifying effects on this axis as seen in the normal population. Sex hormone replacement in Turner's syndrome is associated with normalizing effects on the GH-IGF axis, body composition, physical fitness, and hepatic function. The lowering of hepatic enzymes is a surprising and hitherto undiscovered action of sex steroids. Finally, the route of administration of 17 beta-estradiol is of minor importance in Turner's syndrome.
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PMID:Body composition and physical fitness are major determinants of the growth hormone-insulin-like growth factor axis aberrations in adult Turner's syndrome, with important modulations by treatment with 17 beta-estradiol. 925 36


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