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

---

Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
...
PMID:Differentiation of K562 leukemia cells along erythroid, macrophage, and megakaryocyte lineages. 242 57

Different enzymatic activities were studied in the human pancreatic cancer cell line CAPAN-1 in order to analyze their relation to differentiation. Alkaline phosphatase (Alk Ph), acid phosphatase, aminopeptidase, dipeptidyl peptidase IV, acid and neutral alpha-glucosidases, and acid beta-galactosidase were present. Especially alkaline phosphatase, which we have found to be of the placental type isoenzyme, is being highly expressed. Spontaneous cell differentiation at confluence as well as differentiating agents: sodium butyrate and DMSO, modulated the levels of three enzymes: Alk. Ph., aminopeptidase, and acid alpha-glucosidase. The exposure of the cells to the differentiating agents amplified the modulations occurring during the spontaneous differentiation. Aminopeptidase and acid alpha-glucosidase were found to be induced by differentiation. Alk Ph specific activity was significantly increased by the spontaneous and the butyrate-induced differentiations; whereas DMSO exerted an opposite effect, probably related to its biphasic action on cell proliferation.
...
PMID:Modulation of enzymatic activities during spontaneous and induced differentiation in a human pancreatic adenocarcinoma cell line CAPAN-1. 254 14

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.
...
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

In vitro studies indicate that low concentrations of ethanol can have direct effects on bone formation and resorption. Bone resorption was increased when embryonic chick tibiae were exposed to ethanol at 0.03-0.3% (v/v), and bone formation was inhibited when tibiae were exposed to 0.2% ethanol in the presence of NaF or parathyroid hormone (P less than 0.01 for each). Ethanol also had direct effects on isolated bone cells in vitro, increasing both cAMP and PGE2 production (P less than 0.001 for each), and affecting cell proliferation in a biphasic, time- and dose-dependent manner. After 24 h of exposure, 0.03% ethanol increased bone cell proliferation (P less than 0.001), but 0.3% ethanol was inhibitory (P less than 0.01). Paradoxically, mitogenic doses of ethanol prevented the effects of two other mitogens, NaF and human skeletal growth factor, to increase bone cell proliferation (P less than 0.001). But how were these effects produced? Several observations suggest that these direct effects of ethanol on skeletal tissues in vitro were mediated by changes in bone cell membrane fluidity. (a) Dimethyl sulfoxide, ethylene glycol, and lecithin, which act, like ethanol, to increase membrane fluidity, mimicked the effects of ethanol on bone cell proliferation. Dimethyl sulfoxide also mimicked the effect of ethanol to increase cAMP (P less than 0.001). (b) Cholesterol, which decreases cell membrane fluidity, acted oppositely to ethanol and enhanced the mitogenic response to human skeletal growth factor (P less than 0.001). (c) Preincubation of calvarial cells with ethanol or with cholesterol altered the in situ reaction kinetics of the membrane-bound enzyme, alkaline phosphatase. Together, these data demonstrate that ethanol has direct effects on skeletal tissue in vitro, and suggest that those effects may be secondary to changes in bone cell membrane fluidity.
...
PMID:Direct effects of ethanol on bone resorption and formation in vitro. 298 96

The activities of acid and alkaline phosphatases and phosphotyrosine, phosphoserine and phosphothreonine phosphatases were measured in Friend murine erythroleukaemic (MEL) cells. The effects of treating the cells with dimethyl sulphoxide (DMSO), an inducer of differentiation, were examined. In untreated cells alkaline phosphatase activity was undetectable, though there were significant amounts of acid phosphatase (76 +/- 15 mU/mg protein) and phosphotyrosine phosphatase (16 +/- 0.9mU/mg protein); phosphoserine and phosphothreonine phosphatase activities (9 +/- 0.4 and 7 +/- 0.6mU/mg protein, respectively) were lower than for phosphotyrosine phosphatase. Addition of 1 or 2% DMSO to the culture medium resulted in the expected cell death within 2 weeks. With 0.5% DMSO, cells remained viable for at least 8 weeks, but while some appeared to have smaller nuclei and retained their rounded appearance, others became fibroblastic within several days and adhered to the culture vessel. The treated cells which had kept their morphology showed no difference in acid phosphatase activities as compared with untreated controls; phosphotyrosine phosphatase was lower (9 +/- 0.8mU/mg protein) and phosphoserine and phosphothreonine phophatases higher (11 +/- 0.5 and 10 +/- 0.4mU/mg protein, respectively) than in the controls. The Km values for p-nitrophenyl phosphate were similar in untreated and treated cells (0.069 and 0.068mM, respectively); for phosphotyrosine the Km value was lower in the treated cells (0.97mM) than in the controls (1.9mM).
...
PMID:Acid phosphatase and phosphoamino acid phosphatases in murine erythroleukaemic cells. 298 19

Reactive oxygen species have been found to be responsible for the tissue injury caused in experimental pyelonephritis in mice. The extent of lipid peroxidation (as assayed by malondialdehyde formation) was found to be increased significantly (p less than .001) in the infected group as compared to the normal mice. Superoxide dismutase and catalase (oxygen free radical scavengers) showed a significant decrease (p less than .001) in the extent of lipid peroxidation even in the presence of infection. Dimethyl sulfoxide, a hydroxyl ion scavenger, was however found to be effective only at 4 and 7 days postinfection (p less than .001). Allopurinol, an inhibitor of xanthine oxidase, did not significantly (p greater than .05) inhibit the formation of lipid peroxides, even upto 7 days postinfection. There was a significant decrease (p less than .05) in the activities of renal brush border membrane enzymes used as markers of renal tissue damage (i.e. alkaline phosphatase, leucine amino-peptidase and gamma-glutamyl transpeptidase) in the infected group as compared to the normal group. In the presence of superoxide dismutase, dimethylsulfoxide and catalase except allopurinol, the activities of all the enzymes but maltase were found to be increased significantly (p less than .05) as compared to the infected group. There was a significant increase (p less than .01) in the bacterial count in the presence of superoxide dismutase and DMSO in infected mice as compared to the infected control mice. However, no significant difference was observed in the catalase and allopurinol treated groups.
...
PMID:Effect of various oxygen free radical scavengers in preventing tissue injury caused by Escherichia coli in pyelonephritic mice. 305 56

The effects of 1 mM sodium butyrate or 2% dimethylsulfoxide (DMSO) on three human pancreatic tumor cell lines were examined. The cell lines tested were MIA PaCa-2, PANC-1 and CAPAN-1. Both butyrate and DMSO inhibited the ability of all three lines to form colonies in soft agar. These results suggest that the use of these agents provides a model system for the study of the molecular changes involved in human pancreatic cancer. In butyrate all the cell lines showed a marked increase in cellular levels of alkaline phosphatase, while growth in DMSO led to a reduction in most cases. DMSO caused a rapid reduction in the attachment of all three cell lines to collagen substrates, while butyrate had no effect. These results illustrate the fact that although both butyrate and DMSO appear to greatly reduce the parameters correlated with tumorigenicity of human pancreatic cancer cells, the mechanisms involved may be very different.
...
PMID:Effects of sodium butyrate and dimethylsulfoxide on human pancreatic tumor cell lines. 620 Mar 29

The effects of some high-polar compounds on the cytomorphological characteristics of cultured cells of synovial and osteogenic human sarcomas (Sa-2 and Sa-4) were studied. Incubation of Sa-2 cells with 1 or 2% dimethylsulfoxide (DMSO) or 100 mM dimethylformamide (DMF) during 4-6 days induced the cellular, structural and functional changes in Sa-2 cells which were considered as manifestations of pseudoepithelial differentiation. DMSO did not influence the activity of Sa-2 cell enzymes, while DMF suppressed their activity, mainly that of acid and alkaline phosphatases. DMSO and DMF induced in Sa-4 cultured the appearance of the cells which were similar cytomorphologically to normal osteoblasts. DMSO and DMF significantly depressed the activity of acid phosphatase in Sa-4 cells and transformed the positive reaction of alkaline phosphatase to the negative one. DMSO and DMF prolonged the time of the doubling of Sa-2 and Sa-4 cells. The effects of DMSO and DMF were reversible. Methylformamide (200 mM) and dimethyl acetamide (0,1 and 10 mM) did not induce analogous changes in human sarcoma cells.
...
PMID:[Cytomorphological changes in human tumor cells exposed to high-polar compounds]. 627 49

The protective activity of 1,2-bis(3,5-dioxopiperazin-l-yl)propane (ICRF-187) and dimethyl sulfoxide (DMSO) was tested against acetaminophen-induced hepatotoxicity. Male Syrian golden hamsters injected intraperitoneally between 18:00 h and 20:00 h for 2 consecutive days with acetaminophen (N-acetyl-p-aminophenol) (300 mg/kg) displayed signs of hepatotoxicity as evidenced by increases in enzyme activity and cellular damage. Forty-eight hours after the second acetaminophen dose, the activities of serum glutamic-pyruvic transaminase and alkaline phosphatase were increased compared with levels found in hamsters given only saline. In addition, hepatocellular necrosis was evident in acetaminophen-treated animals. ICRF-187 (300 mg/kg) given 1 h before acetaminophen attenuated the increases in enzyme activities, and both DMSO (7.3 g/kg) and ICRF-187 reduced the incidence and severity of acetaminophen-induced hepatocellular injury. Both ICRF-187 and DMSO are capable of altering free radical-mediated toxicity in other experimental systems. Whether these compounds reduce acetaminophen-induced liver toxicity by a similar mechanism remains to be determined.
...
PMID:Examination of the protective effect of ICRF-187 and dimethyl sulfoxide against acetaminophen-induced hepatotoxicity in Syrian golden hamsters. 641 37

The effects of sodium butyrate, dimethyl sulfoxide (DMSO), and retinoic acid on the growth, morphology, carcinoembryonic antigen content, cell surface membrane-associated enzyme activities, and glycoprotein profiles of a human rectal adenocarcinoma cell line (HRT-18) in culture were compared. All three agents reversibly caused a marked increase in doubling times, a decrease in saturation densities, and a markedly reduced colony-forming efficiency in soft agar. Only butyrate caused gross morphological changes including cell enlargement, flattening, and increased membranous process formation. Carcinoembryonic antigen content was increased during culture in butyrate, while it was reduced by DMSO and unchanged by retinoic acid. The activities of membrane-associated enzymes were altered significantly in the butyrate-treated cells. For example, an increase in the activities of alkaline phosphatase (10-fold), gamma-glutamyl transpeptidase activity (3-fold) and sucrase activity (2-fold) was observed, while those of aminooligopeptidase and K+-stimulated phosphatase actually showed slight decreases. DMSO- or retinoic acid-treated cells showed a marked decrease in alkaline phosphatase activity, but other enzyme activities remained unchanged. Surface protein-labeling patterns of lactoperoxidase-catalyzed iodinated HRT-18 cells showed no significant change from the control cells following treatment with DMSO or retinoic acid. The most prominent change caused by butyrate treatment was the appearance of a major glycoprotein band with an apparent molecular weight of 60,000. These data indicate that the use of butyrate, DMSO, and retinoic acid may provide useful information concerning the identification of differentiation-associated markers of human rectal cancer cells. Furthermore, these agents, although having similar effects on the growth properties, have different effects on the morphology and on the biochemical properties of human rectal cancer cells.
...
PMID:Differential effects of sodium butyrate, dimethyl sulfoxide, and retinoic acid on membrane-associated antigen, enzymes, and glycoproteins of human rectal adenocarcinoma cells. 705 70


<< Previous 1 2 3 4 5 6 7 Next >>

---