Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sodium butyrate causes HeLa cells to assume an elongated and jagged shape. Ultrastructurally this change is associated with the formation of bundles of microfilaments. Desmosomes were present between adjacent cells. No increase in microtubules was observed in the butyrate-treated cells. Butyrate induces an increase in the activity of 2 membrane-bound enzymes, alkaline phosphatase and 5'-nucleotidase; however, the activity of a third membrane enzyme, acetylcholine esterase, is reduced. The activities of the several other enzymes with different subcellular localizations are not significantly increased. Colcemid and cytochalasin B prevent or reverse the butyrate-mediated change in HeLa cell morphology and also partially inhibit the induction of alkaline phosphatase activity in these cells. The effect of cytochalasin B on alkaline phosphatase induction may be caused by a reduction in protein synthesis produced by this fungal metabolite.
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PMID:Ultrastructural and enzymic modulation of HeLa cells induced by sodium butyrate and the effects of cytochalasin B and colcemid. 97 76

Some biological and neurochemical properties of the venom of stonefish (Syanceja horrida) were investigated. The venom exhibited oedema-inducing, haemolytic, hyaluronidase, thrombin-like, alkaline phosphomonoesterase, 5' nucleotidase, acetylcholinesterase, phosphodiesterase, arginine esterase, and arginine amidase activities. Recalcification clotting time, prothrombin, and kaolin-cephalin clotting times were increased 1.7-2.3- and 2.4-fold respectively. The LD50 (i.v. mouse) was 300 micrograms/Kg. Its effects on uptake and stimulation of neurotransmitter synthesis and release were observed in rat brain synaptosomes. In the presence of 100 micrograms venom, uptake of [methyl-3H] choline in rat brain synaptosomes was inhibited 70%, while that of 4-amino-n-[U-14C] butyric acid was inhibited 20%. The toxin also stimulated the release of [3H]-acetylcholine from the synaptosomes.
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PMID:Biological activities of Synanceja horrida (stonefish) venom. 136 68

Sodium butyrate (butyrate), 5-azacytidine (5Aza-C), dimethyl sulfoxide (DMSO), and dimethyl formamide (DMF) were applied to a human melanoma cell line for the purpose of inducing pigmentation and terminal differentiation. The results are summarized as follows: 1) butyrate, DMSO, and DMF had a strong cytostatic effect, arresting cells in the G1 phase of the cycle; 2) butyrate caused a morphological change to spindle shape whereas DMSO and DMF produced rounded cells, without affecting the levels of vimentin and intermediate filaments; 3) tyrosinase activity and melanization were stimulated by DMSO and DMF but not by butyrate; 4) butyrate induced several membrane-bound enzyme activities (alkaline phosphatase and gamma-glutamyl transpeptidase); 5) changes in the expression of antigens related to tyrosinase activity (2B7 and 5C12) only partly corresponded to the changes in enzyme activity; 6) expression of the melanosomal B8G3 antigen was decreased by butyrate, DMSO, and DMF; and 7) the action of DMF resembled that of DMSO whereas 5Aza-C had little effect. The results indicate that these differentiating agents activate different sets of genes, the melanogenic pathway being activated independently of gamma-glutamyltranspeptidase. The down regulation of B8G3 antigen by these agents may provide a common focus for understanding the essential action of differentiation inducers in melanoma cells.
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PMID:In vitro phenotypic alteration of human melanoma cells induced by differentiating agents: heterogeneous effects on cellular growth and morphology, enzymatic activity, and antigenic expression. 171 Mar 61

K562 is a human leukemic cell line used as model of hematopoietic differentiation. A variety of differentiation-inducing agents was used in this study, and the expression of surface membrane antigens associated with specific lineages of differentiation and changes in the cytochemistry of the induced cells were monitored. Sodium butyrate, hemin, retinoic acid, dimethyl sulfoxide (DMSO), phorbol myristate acetate (PMA), and interferon induced unique alterations in the binding of monoclonal antibodies specific for erythroid, granulocytic, monocytic, and megakaryocytic lineages. Hemoglobinization, Sudan Black B, glycogen content, nonspecific esterase, alkaline phosphatase, and 5'-nucleotidase staining were also altered. K562 cells were terminally differentiated with PMA to nitroblue tetrazolium-(NBT) positive macrophages. Expression of 3-fucosyl-N-acetyl lactosamine, previously thought to be myeloid specific but found on all early hematopoietic progenitors, was modulated during differentiation to nonmyeloid lineages. Lineage infidelity was noted during functional differentiation along all hematopoietic lineages. The presence of multiple lineage surface markers and cytoplasmic characteristics in leukemic cells is not indicative of lack of potential to differentiate. K562 cells cannot be compared to any normal stage of hematopoietic differentiation, but they do have the capacity to differentiate along erythroid, macrophage, and megakaryocytic lineages.
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PMID:Differentiation of K562 leukemia cells along erythroid, macrophage, and megakaryocyte lineages. 242 57

The effect of sodium butyrate was examined on the growth and phenotypic expression of a cell line derived from the ascitic fluid of an untreated patient with ovarian carcinoma. The chemical inducer of differentiation, sodium butyrate, markedly enhances the activity of the membrane-bound glycoprotein enzymes, alkaline phosphatase and gamma-glutamyl transpeptidase. The alkaline phosphatase corresponds to placental Regan type. Sodium butyrate (1 mM) alone has only a small inhibitory effect on cell growth. However, it was shown to potentiate the anti-proliferative effect of Adriamycin and to render the cells sensitive to cis-platinum.
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PMID:Sodium butyrate enhances the activities of membranal enzymes and increases drug sensitivity in a cell line from ascitic fluid of an ovarian carcinoma patient. 257 49

Three weeks of butyric acid applications (0.5 g/kg and 1.0 g/kg body weight) caused strong dose-dependent strains on the acid-base balance in young fattening bulls aged 4 months. Disorders were primarily reflected in changed net values of acid-base excretion in urine. Activity of alkaline phosphatase was found to depend strongly and directly on these changes. Drastic variations were recorded also from nitrogen metabolism.
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PMID:[Subacute butyric acid burden in cattle. 2. Effect on the acid-base balance and the protein metabolism in young fattening bulls]. 277 41

Sodium butyrate, at millimolar concentrations, seems to mediate or initiate multiple effects on many mammalian cells in culture. Although many transformed cell lines respond to butyrate treatment with acquisition of normal cellular characteristics, the effect of butyrate on a normal cell type, the parenchymal hepatocyte, has not been studied. Serum-free primary cultures of adult rat hepatocytes maintain many adult characteristics, yet after several days in culture a loss of adult characteristics occurs while fetal characteristics are often reexpressed. Therefore, we investigated whether butyrate treatment would improve the morphologic and biochemical characteristics of cultured hepatocytes. Exposure to 5 mM butyrate for 3 d did not affect hepatocyte viability or morphology but retarded the progressive decline in cytochrome P-450 levels and 5'-nucleotidase activity. The spontaneous increase in alkaline phosphatase activity was reduced and the induction of tyrosine aminotransferase was inhibited after 3 d in culture. The fetal liver characteristic, gamma glutamyltranspeptidase, was not affected by butyrate treatment. Results of this study suggest that butyrate represents a nontoxic compound capable of improving the maintenance of cell culture characteristics of adult rat hepatocytes.
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PMID:Effect of sodium butyrate on primary cultures of adult rat hepatocytes. 288 Aug 33

Sodium butyrate and dimethylsulfoxide (DMSO), two known chemical inducers of cell differentiation, were examined on MCF-7 breast cancer cells. Both agents reduce the proliferative capacity of MCF-7 cells, as reflected by inhibition of colony formation in semisolid agar. Sodium butyrate is shown to enhance markedly the activity of two plasma membrane-bound enzymes, alkaline phosphatase and gamma-glutamyl transpeptidase. DMSO does not enhance the activity of these enzymes, but rather induces a small decrease in gamma-glutamyl transpeptidase activity. The present results show that although both agents inhibit cell proliferation, they have a distinct effect on phenotypic expression.
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PMID:Differential effects of sodium butyrate and dimethylsulfoxide on gamma-glutamyl transpeptidase and alkaline phosphatase activities in MCF-7 breast cancer cells. 289 May 41

We have studied the effects of sodium butyrate, retinoic acid, and dimethyl sulfoxide on two human ovarian carcinoma cell lines PE04 and PE01. PE04 cells, after treatment with sodium butyrate at cytostatic doses (2-3 mM for 4 days), exhibited phenotypic changes including induction of alkaline phosphatase and determinants recognized by the monoclonal antibodies 123C3 and 123A8. These effects are not simply the result of cytostasis as they were not produced by dimethyl sulfoxide or retinoic acid. Other markers are also modified by sodium butyrate including lipid, acid mucin, and glycogen. Retinoic acid modulated expression of lipid and CA125, while dimethyl sulfoxide reduced expression of CA125. Other short chain fatty acids such as propionic acid and valeric acid (in addition to butyric acid) also induced alkaline phosphatase and the determinants recognized by 123C3 and 123A8 in PE04 cells. Other differentiation inducers and cytotoxic agents studied did not induce these markers at cytostatic concentrations. The effects of sodium butyrate (and related short chain fatty acids) thus appear to be relatively specific for this cell line.
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PMID:Effect of sodium butyrate and other differentiation inducers on poorly differentiated human ovarian adenocarcinoma cell lines. 316 62

The incidence, distribution, size, and histopathology of small and large bowel tumors induced by parenteral administration of 1,2-dimethylhydrazine were examined in rats given 1% or 2% sodium butyrate dissolved in drinking water. Although previous in vitro reports on colon cancer cell lines have suggested that sodium butyrate might have a role to play as a chemotherapeutic "differentiating agent," the results of this in vivo study indicate that sodium butyrate treatment enhanced the development of colonic neoplasia and was associated with increased fecal butyric acid concentrations. In contrast, no changes were seen in the incidence of small bowel tumors, luminal butyric acid concentrations, mucosal morphology, or brush-border enzyme activities (i.e., sucrase, alkaline phosphatase). This study suggests that dietary butyrate has an important, possibly indirect, regulatory role in carcinogenesis associated with an experimental animal model of colonic neoplasia.
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PMID:Effects of differing concentrations of sodium butyrate on 1,2-dimethylhydrazine-induced rat intestinal neoplasia. 373 64


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