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)

Cytochemical indices of leukocytes were determined in 16 patients with diabetes mellitus in the period of unbalancing and balancing. The following tests were made: content of glycogen and lipids, acid phosphatase (AP), alkaline phosphatase (AIP), myeloperoxidase (MPO) and nonspecific alpha-naphtol acetate esterase (NANAE) activity. In unbalanced diabetics an evident decrease in the activity of AP and MPO could be noted as well as a decrease of glycogen content and an increase of lipid content. An insignificant decrease could be observed in the activity of ALP and NANAE in granulocytes. A slight increase in the activity of NANAE in monocytes would be found. Balancing this disease induced the increase of all parameters in granulocytes except MPO activity. It is interesting to note that balancing diabetes mellitus deepened the observed changes in the decrease or increase of tested parameters. The presented findings clearly indicate the role of metabolic disorders in diabetes mellitus on the activity of some neutrophilic enzymes and the glycogen and the content of lipids in neutrophils.
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PMID:Cytochemical indices of leukocytes in patients with diabetes mellitus. 258 66

Intrahepatic cholestasis associated with severe extrahepatic bacterial infection is well recognized in humans. A similar syndrome is not well characterized in veterinary medicine. Five dogs with severe extrahepatic bacterial infection that developed histologically confirmed intrahepatic cholestasis were selected from the authors' case files. The types of infections included pneumonia, peritonitis secondary to a rectal tear, urinary tract infection, bite wounds, and vegetative endocarditis. Escherichia coli was involved in two of the dogs, mixed infection in one dog, and a gram-positive cocci in the other two dogs. Total bilirubin concentrations ranged from 3.5 to 33.5 mg/dl. Serum liver enzyme activities showed only mild to moderate increases: alkaline phosphatase (ALP, 41-750 IU/l), alanine aminotransferase (ALT, 25-235 IU/l), and aspartate aminotransferase (AST, 99-255 IU/l). Fasting serum bile acids concentration was markedly elevated in the one dog in which it was measured (259 mumol/l). Histologically, the cholestasis was characterized by bile pigment accumulation in hepatocytes, canaliculi, and/or Kupffer's cells. Inflammatory parenchymal changes, when present, were minimal. The findings of hyperbilirubinemia, only a slight increase in the liver enzyme activities, and minimal inflammatory changes in liver tissue specimens in the five dogs with extrahepatic bacterial infections are similar to the findings in intrahepatic cholestasis associated with extrahepatic bacterial infection in humans.
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PMID:Cholestasis associated with extrahepatic bacterial infection in five dogs. 258 68

Hypophosphatasia is a heritable disorder characterized by defective osteogenesis and deficient liver/bone/kidney alkaline phosphatase (L/B/K ALP) activity. Severe forms of the disease are inherited in an autosomal recessive fashion. We examined cultured skin fibroblasts from twelve patients with severe hypophosphatasia. All were deficient in L/B/K ALP activity, yet produced normal levels of the corresponding mRNA. Sequence analysis of L/B/K ALP cDNA isolated from one of the patient-derived fibroblast lines revealed a point mutation that converted amino acid 162 of mature L/B/K ALP from alanine to threonine. The patient was homozygous and the parents, who are second cousins, heterozygous for this mutation. Introduction of the mutation into an otherwise normal cDNA disrupted the expression of active enzyme, demonstrating that a defect in the L/B/K ALP gene resulted in hypophosphatasia and that the enzyme is, therefore, essential for normal skeletal mineralization.
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PMID:First identification of a gene defect for hypophosphatasia: evidence that alkaline phosphatase acts in skeletal mineralization. 260 56

Significant decreases in magnesium (Mg) concentration and alkaline phosphatase (ALP, EC 3.1.3.1) activity in serum were seen in patients after cardiac surgery with cardiopulmonary bypass (Group 1), as compared with non-cardiac-surgery patients after general anesthesia (Group 2) or only spinal anesthesia (Group 3). Mean changes for Mg and ALP by the first postoperative day, compared with pre-operative baseline values, were as follows: Group 1: Mg -7.5 mg/L (-38.3%), ALP -46U/L (-48.4%); Group 2: Mg -3.3 mg/L (-17.4%), ALP -17 U/L (-16.5%); and Group 3: Mg -1.9 mg/L (-10.0%), ALP -15 U/L (-14.0%). The decreases in Mg and ALP observed in post-cardiac-surgery patients appear to be a consequence of the cardiac surgery and the cardiopulmonary bypass pump. Measurement of Mg and ALP in a subgroup of 10 cardiac-surgery patients for 10 days postoperatively showed initial decreases, with gradual recovery to near-normal values by the 10th day. That the changes in Mg and ALP seen postoperatively were not attributable to hemodilution alone was confirmed by measuring total-protein concentrations before and after operation. ALP requires Mg ion in vitro for optimal activity, but addition of Mg in the appropriate amounts to sera with low ALP activity did not restore ALP activity. The low ALP activity seen in post-cardiac surgery patients in vivo may perhaps be related to factors other than Mg that were removed by the cardiopulmonary bypass pump.
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PMID:Hypomagnesemia and low alkaline phosphatase activity in patients' serum after cardiac surgery. 270 51

Hypophosphatasia is a heritable disorder characterized by defective bone mineralization and a deficiency of liver/bone/kidney alkaline phosphatase (L/B/K ALP) activity in serum and tissues. Severe forms of the disease, which are generally lethal in infancy, are inherited in an autosomal recessive fashion. The gene defects that produce hypophosphatasia are poorly understood, but many are likely to occur at the L/B/K ALP locus. To investigate these gene defects, we analyzed L/B/K ALP DNA, RNA, and enzyme activity in cultured dermal fibroblasts from 14 patients with perinatal or infantile hypophosphatasia and from 12 normal individuals. Southern blot analyses of the L/B/K ALP genes from patients and controls revealed identical restriction patterns. Control fibroblast ALP activity correlated with the corresponding L/B/K ALP mRNA levels estimated by blot hybridization analysis and densitometry (r = .94, P less than .0001). In contrast, fibroblasts from the hypophosphatasia patients were deficient in ALP enzyme activity but expressed apparently full-sized L/B/K ALP mRNA at normal levels. Bone specimens from one of the patients were examined and found to be deficient in histochemical ALP but contained immunologic cross-reactive material detected by anti-human liver ALP antiserum. Our results demonstrate that the deficiency of ALP activity in fibroblasts from 14 patients with severe hypophosphatasia is not due to decreased steady-state levels of the corresponding mRNA. The presence of enzymatically inactive L/B/K ALP protein in one of these patients is consistent with a point mutation or small in-frame deletion in the coding region of L/B/K ALP gene.
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PMID:Analysis of liver/bone/kidney alkaline phosphatase mRNA, DNA, and enzymatic activity in cultured skin fibroblasts from 14 unrelated patients with severe hypophosphatasia. 270 56

The purpose of this study is to investigate the immunological difference between intestinal, liver, kidney, bone, placental and serum alkaline phosphatase (ALPs) in cattle. Kidney, bone and placental ALPs were purified from each tissue by gel filtration and ion-exchange chromatographies, and intestinal, liver, and placental ALPs were obtained from a commercial source. The antibody to each tissue ALP was prepared by immunizing rabbits and tested by double immunodiffusion analysis in cross reactivities. The results indicated that the bovine tissue ALPs are divided into four groups in antigenicity, that is, intestinal, bone, liver and kidney-placental ALPs. The fetus, calf and cow sera contained bone ALP, and calf and cow sera also contained kidney or placental ALP, but all of the sera did not contain intestinal and liver ALP.
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PMID:Immunological investigation of intestinal, liver, kidney, bone, placental and serum alkaline phosphatase in cattle. 273 6

Alkaline phosphatase (ALP; EC 3.1.3.1) isoenzymes were measured in the plasma of 63 untreated hyperthyroid patients (the hyperthyroid group), 58 treated hyperthyroid patients, and 100 blood donors. Total, liver, and bone ALP activities were significantly higher in the hyperthyroid group than in the treated hyperthyroid group or the blood donors. Bone ALP was more frequently and more markedly abnormal than liver ALP. Intestinal ALP did not differ significantly between the groups. The hyperthyroid patient group had significantly higher plasma calcium concentrations and lower serum parathyrin concentrations than those of the treated hyperthyroid group.
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PMID:Alkaline phosphatase isoenzymes in plasma in hyperthyroidism. 275 88

The different distribution of cytochemically demonstrable enzymes: lactate dehydrogenase (LDH, 1.1.1.27), succinate dehydrogenase (SDH, 1.3.99.1), dihydrofolate reductase (DHFR, 1.5.1.3), acid phosphatase (AcP, 3.1.3.2) and alkaline phosphatase (ALP, 3.1.3.1), has been documented in Yoshida ascites hepatoma cells in vivo or stored at 80 degrees C. The dehydrogenase activities (LDH, SDH, DHFR) show a strong reaction in all samples. An increased level of these enzyme activities has been observed in the malignant cells spreading through the organs of tumor bearing rats. On the contrary, in the same samples, acid and alkaline phosphatase activities are very low. The strong dehydrogenase activities observed in Yoshida ascite cells stress the rapid turnover of tumor cells. Our results indicate that the histochemical method may be a useful tool to detect the scattered tumor cells. Furthermore, the cytochemical methods allow the characterization of the metabolic pathways employed by the primary and disseminated tumor cells.
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PMID:[Cytochemical study of cells of primary and disseminated ascite Yoshida tumor cells]. 276 51

Bone alkaline phosphatase (B-ALP) and tartrate resistant acid phosphatase (TR-ACP) are markers of osteoblastic and osteoclastic activities respectively. During a period of up to two years, these isoenzymes have been assayed in the sera of 191 breast cancer patients; 80 had bone metastases (BM). In BM bearing patients, B-ALP activity was 261 IU/l and 63 IU/l for patients without BM; TR-ACP was respectively 6.6 and 3.3 IU/l. Specificity and sensitivity were calculated according to several criteria. These isoenzyme serum levels were well correlated with those of two breast cancer markers (CEA and CA15.3) and radiograph.
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PMID:Isoenzymes of alkaline and acid phosphatases as bones metastasis marker in breast cancer patients. 281 92

This paper describes in vitro studies on the effects of environmental pollutants (SO2/NOx) in biological systems. Basic physical, chemical and biochemical parameters were analyzed to establish the rate of SO2/NOx absorption by the culture medium. It was shown that the pH remains constant for 24 h of exposure to gas concentrations up to 50 p.p.m. The concentration of ions resulting from absorption of each pollutant in the liquid phase is dependent on their concentration in the gas phase and on exposure time. Short exposure times and high gas dosages resulted in similar doses in the medium as long exposure periods and low gas dosages. The activities of a human serum standard (alkaline phosphatase, ALP; aspartate amino transferase, AST; alanine amino transferase, ALT; gamma-glutamyltransferase, gamma-GT; lactate dehydrogenase, LDH) were determined after gaseous exposure to SO2 and NOx. The results revealed a distinct decrease in the activity of LDH after 1, 3 and 5 h exposure to 200 p.p.m. SO2. The effects of the pollutants were assayed in vitro using fetal hamster lung cells (FHLC), rat hepatocytes and the cell line CO60. For the determination of toxic effects, it was shown that the plating efficiency was a more sensitive parameter than the assay for trypan blue exclusion. Toxicity indicated as an increase of LDH leakage was not observed from FHLC in culture. Instead, a decrease of LDH was found following SO2 exposition. This decrease was similar to that observed for the human serum standard. The induction of DNA single-strand breaks was determined as a measure of genotoxic effects. SO2 application decreased the rate of DNA single-strand breaks induced by N-nitroso-acetoxymethyl-methylamine in both FHLC and in rat hepatocytes. SO2 or NOx treatment of CO60 cells for 1 h did not result in the induction of DNA amplification. HSO3- added directly to the medium as the sodium salt, however, distinctly induced the amplification of SV40 DNA. The amplification rates induced by benzo[a]pyrene or dimethylbenzanthracene were neither influenced by SO2, NOx nor HSO3-. An additive effect of HSO3- with either benzo[a]pyrene or dimethylbenzanthracene for this biological parameter was therefore not observed.
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PMID:Effects of SO2 or NOx on toxic and genotoxic properties of chemical carcinogens. I. In vitro studies. 283 97


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