Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.11.1.7 (peroxidase)
 65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present studies were carried out to clarify the mechanism of glucagon choleresis in guinea pigs. At the infusion rate of 1.4 nmol.min-1.kg-1, glucagon increased bile flow from 206.6 +/- 14.3 to 302.6 +/- 35.0 microliters.min-1.kg-1 and bicarbonate biliary concentration from 63.7 +/- 4.2 to 75.5 +/- 5.9 meq/l. Measurements of bile acid excretion in bile, the biliary tree volume, and of the hormone choleretic effect in guinea pigs with proliferated bile ductules/ducts induced by alpha-naphthylisothiocyanate feeding indicated that glucagon, unlike secretin, stimulated canalicular bile flow. Inhibition of prostaglandin synthesis by indomethacin administration (5 mg.kg-1.h-1) did not modify the choleretic effect of glucagon, and infusion of a glucagon analogue (TH-glucagon, 1.4 nmol.min-1.kg-1), which did not increase hepatic formation of adenosine 3'5'-cyclic monophosphate (cAMP), failed to stimulate bile flow. Like the parent hormone, however, TH-glucagon augmented plasma glucose levels and stimulated formation of inositol phosphates. Colchicine pretreatment (0.5 mg/kg ip) almost entirely prevented the choleretic effect of glucagon but did not modify spontaneous and bile acid-induced bile flow and the stimulatory effect of the hormone on glucose release and on hepatic formation of cAMP and inositol phosphates. Finally, glucagon produced a large increase in the biliary entry of horseradish peroxidase, even though this effect was transient and was not coupled to the increase in bile flow. These results indicate that glucagon choleresis in the guinea pig is not secondary to prostaglandin release, is canalicular in origin, involves bicarbonate secretion, is mediated by cAMP, and requires an intact microtubular system.
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PMID:mechanism of glucagon choleresis in guinea pigs. 217 15

The diminished basal tear flow in aged individuals is associated with lymphocytic infiltrations and atrophy of the lacrimal ducts and acini. We have investigated the age-related physiological changes to sympathomimetic stimulation of lacrimal tissue from F344 rats to determine if the responses are uniformly diminished as would be expected by glandular atrophy. The quantitative and temporal pattern of protein and peroxidase secretion by lacrimal gland fragments from young (4 month) and aged (24 month) F344 male rats was examined in a perifusion system. Upon stimulation of tissue from young animals with 0.01 mM phenylephrine for 40 min, secretion above baseline levels of protein was 570.8 micrograms/g tissue and of peroxidase was 45.2 delta A X min-1/g tissue. The response of the aged tissue to phenylephrine was not significantly different from that of the young tissue. beta-adrenergic stimulation by isoproterenol (0.01 mM) evoked only a modest secretion of protein and no consistently measurable peroxidase from young tissue. IBMX alone and in combination with isoproterenol (0.1 mM and 0.01 mM respectively) evoked a large secretion of protein, 1345.7 micrograms/g tissue, and a modest secretion of peroxidase, 9.5 delta A X min-1/g tissue by young tissue. The aged tissue, upon stimulation with the combination of IBMX and isoproterenol, secreted significantly less protein and peroxidase than the young tissue. In separate experiments, the production of cAMP was measured. In young tissue, isoproterenol did not cause a measurable increase of intracellular cAMP. IBMX caused a 2-3 fold increase in cellular cAMP which was not increased further by addition of isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathomimetic protein secretion by young and aged lacrimal gland. 242 79

In an attempt to assess the effect of alcohol per se on human polymorphonuclear neutrophils (PMN), irrespective of other physiopathological parameters, we examined neutrophil function in healthy volunteers who had taken a single large dose of whisky. Before and at different times after ingestion, several PMN properties were simultaneously tested including random migration, in vitro chemotaxis, adherence, aggregation, cytochrome C reduction, phagocytosis, bacterial killing, intracellular cAMP and cGMP contents, myeloperoxidase, and neutrophil alkaline phosphatase scores. Only phagocytosis of Staphylococcus aureus was significantly depressed after alcohol ingestion. Adherence was inhibited only in some individuals when their respective blood alcohol levels were the highest. Both alterations were moderate and reversible. These data point out the limited effect of occasional alcohol consumption on the different facets of neutrophil behavior. These findings suggest that factors other than alcohol itself could be concerned in the marked PMN dysfunction well established in chronic alcoholism.
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PMID:Human neutrophils are not severely injured in conditions mimicking social drinking. 255 61

The regulation of trophoblast secretion of the placental proteins CG (hCG), placental lactogen (hPL), and pregnancy specific-beta-1-glycoprotein (SP-1) has not been fully elucidated. We therefore studied the secretion of hCG, hCG-beta subunit, hCG-alpha subunit, hPL, and SP-1, both in the basal state and after exposure to 8-bromo-cAMP, during the in vitro differentiation of cytotrophoblasts to syncytiotrophoblasts. Term placental tissue was enzymatically digested and cytotrophoblasts purified by Percoll density gradient centrifugation. At the time of seeding of 4-6 X 10(5) cells/ml in 35-mm flasks all of the cells were mononuclear and 48% contained hCG-alpha, but none contained hCG or hCG-beta by the avidin-biotin-peroxidase immuno-histochemical method. After 3 days in culture, hCG-alpha and hCG or hCG-beta were present in multinucleated syncytiotrophoblasts and in the mononuclear cytotrophoblasts. During the 5 days in culture, the secretion of hCG, hCG-alpha, hPL and SP-1 into the media increased and reached a maximum on day 4 followed by a decrease on day 5. Basal hCG-beta secretion was very low and did not change during culture. The ratio of hCG-alpha/hCG decreased from days 1-4 of culture. Incubation with 8-bromo-cAMP for 24 h stimulated the secretion of hCG and hCG-alpha, whereas hCG-beta and hPL levels did not change. The secretion of SP-1, however, was inhibited by 8-bromo-cAMP. These results indicate that the cytotrophoblasts secrete hCG, hCG-beta and hCG-alpha during in vitro differentiation into syncytiotrophoblasts. Since the basal ratio of hCG to hCG-alpha secretion changed during 5 days in culture and a cAMP analogue differentially modulated the secretion of the different placental protein hormones, the physiological regulation of secretion of each of the proteins also may differ.
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PMID:Discordant secretion of placental protein hormones in differentiating trophoblasts in vitro. 264 16

A rat thyroid peroxidase cDNA has been isolated from a FRTL-5 thyroid cell library and sequenced. The cDNA is 2776 base pairs long with an open reading frame of 770 amino acids. By comparison to full-length human thyroid peroxidase cDNA and based on its identification of a 3.2 kilobase mRNA in rat thyroid FRTL-5 cell Northern blots, the rat peroxidase cDNA appears to lack 400-500 base pairs at the 5'-end of the mRNA. It exhibits only a 74% nucleotide and 77% amino acid sequence similarity to human thyroid peroxidase cDNA within the total aligned sequences, although the predicted active site regions are highly conserved (greater than 90-100%). The cDNA has been used to map the thyroid peroxidase gene in mice to chromosome 12 and to compare thyroid peroxidase and thyroglobulin gene expression in FRTL-5 rat thyroid cells. Despite the fact TSH action in both cases is duplicated, and presumably mediated, by cAMP, TSH-induced increases in thyroid peroxidase and thyroglobulin mRNA levels differ. Differences exist with respect to hormone concentration and time. The ability of TSH to increase thyroglobulin, but not thyroid peroxidase mRNA levels, requires insulin, 5% serum, or insulin-like growth factor-I. Insulin or insulin-like growth factor-I alone can increase thyroglobulin mRNA levels as well as or better than TSH but have only a small effect on thyroid peroxidase mRNA levels by comparison to TSH. The ability of TSH to increase thyroglobulin gene expression is readily detected in nuclear run-on assays but not the ability of TSH to increase thyroid peroxidase gene expression. Cycloheximide inhibits TSH-increased thyroglobulin but not peroxidase mRNA levels. Finally, methimazole and phorbol 12-myristate 13-acetate show different effects on TSH-induced increases in thyroglobulin and thyroid peroxidase mRNA levels.
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PMID:Thyroid peroxidase: rat cDNA sequence, chromosomal localization in mouse, and regulation of gene expression by comparison to thyroglobulin in rat FRTL-5 cells. 269 80

Neutrophil-mediated antibody-dependent cellular cytotoxicity (ADCC) against Raji target cells and neutrophil degranulation during the ADCC process were evaluated in the presence and in the absence of different agents able to interfere with the neutrophil release of granule components (anion channel blockers, colchicine, isoproterenol, dimethylxanthine, cAMP). When used at concentrations incapable of preventing the target cell recognition by neutrophils, the majority of these agents inhibited both the ADCC and the release of myeloperoxidase (MPO, primary granule marker) and lysozyme (LZM, primary and secondary granule marker). The inhibition of the ADCC correlated strictly with the inhibition of the MPO release. Thus, the results are consistent with the hypothesis that neutrophil primary granules play a major role in the cytolytic process.
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PMID:Relationship between antibody-dependent tumour cell lysis and primary granule exocytosis by human neutrophils. 282 22

Cytochalasin D altered the kinetics of peroxidase and radiolabeled protein discharge from rat exorbital lacrimal glands in vitro, in response to various secretagogues. The changes were different with each inducer. The discharge due to isoproterenol was immediately inhibited by 95%; the discharge evoked by noradrenaline via alpha-adrenergic receptors was progressively reduced and was inhibited by 50% after 30 min, whereas that evoked by carbachol was not influenced during the initial discharge period and was diminished by only 30% after 30 min. When calcium was removed from the incubation medium, the secretory responses were lowered and the inhibitory effect of cytochalasin D was still observed. The rate of protein discharge inhibition was related to the dose and was maximal with 2 X 10(-6) M cytochalasin D when the discharge resulted from cholinergic, alpha- or beta-adrenergic or dibutyryl cAMP stimulation. Cytochalasin D did not impair cellular energetics nor other stimulations induced through muscarinic or adrenergic receptors. Cytochalasin D effects could be related to interaction with actin, leading to the inhibition of the release of proteins into the incubation medium following the activation of the adrenergic system.
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PMID:Comparative effects of cytochalasin D on the protein discharge induced by alpha- and beta-adrenergic or cholinergic agonists in rat exorbital lacrimal glands. 285 78

Mouse liver mRNA enriched in sequences coding for liver phosphofructokinase by polysome immunoadsorption was used as a template for the synthesis of cDNA. The double-stranded cDNA was inserted into the expression vector lambda gt11 and cloned. Preliminary identification of clones containing cDNA sequences for phosphofructokinase was made by screening the library with anti-rat liver phosphofructokinase serum and horseradish peroxidase-conjugated goat anti-rabbit IgG as second antibody. Subsequently, by selecting antibodies specific to fusion proteins expressed by putative clones and by reacting with Western blots of mouse liver proteins several clones were positively identified as containing liver phosphofructokinase sequences. A cDNA clone corresponding to 2708 nucleotides of liver phosphofructokinase mRNA was further characterized and sequenced. The liver phosphofructokinase mRNA has an open reading frame of 2343 nucleotides followed by a 3'-untranslated region of 303 nucleotides. The G/C-rich (76%) portion of the 5'-untranslated region precedes a characteristic translational start site of CCGCC(AUG). The mRNA coding sequence indicates that the liver phosphofructokinase subunit is composed of 780 amino acid residues and has a Mr of 85,000. Comparison of the deduced amino acid sequence of mouse liver phosphofructokinase with the known rabbit muscle phosphofructokinase shows 68% homology. The N-half of the liver phosphofructokinase has conserved substrate binding sites for ATP and fructose-6-P. The 25 C-terminal residues, which contain the ATP inhibitory site, are the least homologous (20%) but contain a putative phosphorylation site (Arg-Arg-X-X-Ser). The liver phosphofructokinase mRNA is under nutritional and hormonal regulation. The liver phosphofructokinase mRNA level increased 4-fold when previously starved mice were refed a high carbohydrate, fat-free diet. This increase in mRNA level was blocked by 50% by the administration of dibutyryl cAMP. The induction of liver phosphofructokinase mRNA by fasting/refeeding was also diminished in streptozotocin diabetic mice.
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PMID:Liver (B-type) phosphofructokinase mRNA. Cloning, structure, and expression. 296 93

Retinoic acid induces differentiation of embryonal carcinoma F9 cells into parietal endoderm. The surface proteins of F9 cells from induced and control cultures were labeled with the 125I-lactoperoxidase system and analyzed by two-dimensional gel electrophoresis. Their quantitative comparison has shown an 11-fold increase of protein p220 of apparent MW 220,000 and isoelectric point 5.6. Among other enhanced surface proteins, 3.5-fold increases of p50, p45, and p40 of MW 50,000-40,000 and isoelectric point 5.1-5.3 were observed. Simultaneously another surface protein, p70 of MW 70,000 and isoelectric point 6.1-6.3, disappeared. The quantitative changes of surface proteins produced after treatment with retinoic acid were enhanced in the presence of dibutyryl cAMP. Analysis of lectin-binding proteins demonstrated that increasing proteins p220, p50, p45, and p40 have an affinity for concanavalin A, whereas p70, which decreases, has an affinity for wheat germ agglutinin. Antibodies raised against p70 from undifferentiated cells have shown a specific immunoreaction with p220 from differentiated cells and also with the subunit B of purified laminin. The electrophoretic mobilities of p220 and of the B subunit of laminin are similar. It is suggested that p70, p220, and laminin B subunit share structural homology.
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PMID:Changes of surface glycoproteins after retinoic acid-dibutyryl cAMP-induced differentiation of teratocarcinoma stem cells. 300 43

We have investigated the effect of methimazole (MMI) on cell-mediated immunity and ascertained the mechanisms of immunosuppression produced by the drug. Methimazole (greater than or equal to 10(-5) M) produced a dose-dependent inhibition in 'active' (early) rosette formation with sheep red cells and in phytohaemagglutinin (PHA)-induced lymphocyte transformation. A concentration of 10(-4) M MMI inhibited the immediate rise in intracellular cAMP triggered by PHA and the subsequent time dependent decrement over 24 h. The drug (10(-3) M) also exerted a significant inhibitory effect on antibody-dependent cell-mediated cytotoxicity (ADCC) over six-fold difference in target/effector cell ratios. At a concentration of 10(-5) M, MMI inhibited zymosan-induced respiratory burst (determined by change in the chemiluminescence of oxidized luminol) in polymorphonuclear and mononuclear cell preparations. Ninety-five per cent of the chemiluminescence in the latter preparation was due to monocytes. At concentrations between 10(-7) and 10(-6) M, MMI significantly inhibited (in cell-free systems) horseradish peroxidase-dependent generation of chemiluminescence as well as the oxidation of luminol by hydrogen peroxide. Methimazole exerts its inhibitory effects on measures of cell-mediated immunity by at least two mechanisms: inhibition of peroxidase and scavenging free oxygen radicals. Insensitivity of the test systems or poor access of MMI to leucocytes may account for the need for greater than or equal to 10(-5) M MMI to inhibit cell-mediated immunity significantly.
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PMID:The immunosuppressive effect of methimazole on cell-mediated immunity is mediated by its capacity to inhibit peroxidase and to scavenge free oxygen radicals. 302 72


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