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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mediator release from rat peritoneal and human lung mast cells as well as human leukemic basophils was examined to determine whether super-oxide (O(-) (2)) was concomitantly generated. Immunologic or nonimmunologic stimulation of each preparation induced parallel release of histamine and O(-) (2) within 2 min. O(-) (2) production was quantitated by superoxide dismutase (SOD)-inhibitable chemiluminescence and cytochrome c reduction. SOD was detected in basophil and mast cell lysates and was also released by rat mast cells stimulated by anti-IgE. Secretory granules isolated from purified rat mast cells released histamine, O(-) (2), and SOD upon exposure to cations. Thus, both superoxide radicals and SOD may play a role in host defenses involved in immediate hypersensitivity reactions.
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PMID:Immunologic and nonimmunologic generation of superoxide from mast cells and basophils. 7 48

In this study data are presented on the kinetics of changes in malondialdehyde content (MDA), lipoxygenase activity (LO), superoxide dismutase activity (SOD), glutathione peroxidase activity (GSH-Px) and glutathione reductase activity (GSSG-Red) during the course of histamine secretion from rat mast cells. Both receptor-mediated (antigen, polymyxin B, compound 48/80) and non-receptor (the calcium ionophore A23187) stimuli of mast cell activation were investigated. A similar alteration in all the studied indices was observed after challenge with receptor-mediated stimuli. The earliest event was a decrease in SOD-activity, which coincided with the increase in histamine secretion. SOD-activity then gradually increased above the baseline levels. Similar changes in GSSG-Red- and GSH-Px-activities were also observed. The increase in MDA content occurred slightly later. Challenge with the calcium ionophore A 23187 did not cause a reduction in SOD-activity, only the increase in activity was observed. Histamine release induced by all stimuli was accompanied by a marked elevation in enzymatic peroxidation (LO-activity). Diethyldithiocarbamate (DTC), which inhibits SOD, not only blocked the enzyme activity but also caused a dose-dependent inhibition of histamine release and an inhibition of the elevation of enzymatic peroxidation in mast cells challenged with compound 48/80.
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PMID:Kinetics of oxygen metabolism indices in the course of histamine secretion from rat mast cells. 169 69

Experiments were carried out to provide evidence of the effect of L-arginine (L-Arg), its analogue NG-monomethyl-L-arginine (MeArg) and of some nitrovasodilators (sodium nitroprusside, NaNP; 3-morpholino-sydnonimine, SIN-1) which spontaneously release nitric oxide (NO) on ischemia-reperfusion injury, histamine release and mast cell degranulation, occurring after multiple ligature and release of the left anterior descending (LAD) coronary artery in isolated perfused guinea-pig hearts. The reopening of the LAD coronary artery leads to a release of histamine related to a decrease in microdensitometry of cardiac mast cells and to calcium overload. The perfusion of the heart with NO-donors significantly reduces either the release of histamine, the loss of mast cell metachromasia and the overload of calcium. These effects were potentiated by SOD. The results suggest that the endogenous formation of NO and molecules able to generate NO have a role in the prevention of post-ischemic tissue injury.
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PMID:The effect of nitric oxide generators on ischemia reperfusion injury and histamine release in isolated perfused guinea-pig heart. 171 36

Rat serosal mast cells were evaluated for their capacity to generate a nitric oxide-like factor by two bioassays: inhibition of platelet aggregation and stimulation of mast cell guanylate cyclase. Incubation of mast cells with human washed platelets, both treated with indomethacin, inhibited thrombin-induced platelet aggregation which was potentiated by superoxide dismutase and reversed by oxyhaemoglobin. When mast cells alone were stirred at 1000 rpm, a time dependent increase in the levels of their cGMP but not cAMP was observed. Preincubation of mast cells with NG-monomethyl-L-arginine significantly enhanced E. coli lipopolysaccharide-evoked histamine release. Our results show that mast cell histamine release can be modulated by an intrinsically generated nitric oxide-like factor.
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PMID:Rat mast cells synthesize a nitric oxide like-factor which modulates the release of histamine. 171 38

In an ischemia-reperfusion model obtained in isolated perfused guinea pig heart by means of a double ligature of the left anterior descending coronary artery, the reperfusion of the ischemic myocardium leads to a release of lactate dehydrogenase and histamine, related to a decrease in the microdensitometry of cardiac mast cells and to a tissue calcium overload. The perfusion of the heart with L-arginine and with nitric oxide donors significantly reduces the release of histamine, the loss of mast cell metachromasia and calcium overload. These effects were potentiated by superoxide dismutase.
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PMID:Effect of nitric oxide generators on ischemia-reperfusion injury and histamine release in isolated perfused guinea pig heart. 171 88

Rat serosal mast cells were tested for their ability to generate a nitric oxide-like factor by two bioassay systems: inhibition of platelet aggregation and stimulation of mast cell guanylate cyclase. Incubation of rat serosal mast cells with human washed platelets resulted in an inhibition of thrombin-induced platelet aggregation proportional to the number of cells. The inhibition was potentiated by superoxide dismutase (SOD) and reversed by oxyhaemoglobin (oxyHb). The inhibitory activity of mast cells was also prevented by NG-monomethyl-L-arginine (MeArg), an effect reversed by co-incubation with L-Arg but not D-Arg. When mast cells alone were stirred at 1,000 rpm, a time-dependent increase in the levels of their cGMP but not cAMP was observed. This increase was reduced by pretreatment with MeArg. The inhibitory effect of MeArg was reversed by L-Arg but not D-Arg. These results demonstrate that rat mast cells release a factor with the same pharmacological profile as NO, and that this NO-like factor is derived from L-arginine.
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PMID:Synthesis of a nitric oxide-like factor from L-arginine by rat serosal mast cells: stimulation of guanylate cyclase and inhibition of platelet aggregation. 197 20

Alveolar macrophages (AMs) and mast cells reside in the airway, and both have been demonstrated to contribute independently to allergic inflammatory responses through the generation of respiratory-burst metabolites and the release of biologically active mediators, respectively. Since mast cell granules (MCGs) contain mediators that could potentially interact with the AM respiratory burst, we investigated the effects of isolated MCGs on this important inflammatory pathway of the AM. MCGs and AMs were obtained by peritoneal and tracheoalveolar lavage, respectively, of Sprague-Dawley rats. First, the overall respiratory-burst activity was measured by luminal-enhanced chemiluminescence (CL), and second, the individual oxygen species contributing to CL (superoxide anion [O2-], hydrogen peroxide [H2O2], and hypochlorous acid) were measured. MCGs alone enhanced AM CL responses to an equivalent degree compared to zymosan-stimulated AMs. However, AMs preincubated with MCGs followed by zymosan stimulation significantly and synergistically enhanced the CL responses. This enhanced CL was not due to an increased production of O2-, H2O2, or hypochlorous acid; in fact, there were decreased measured amounts of O2- and H2O2 from zymosan-stimulated AMs in the presence of MCGs, most likely caused by the content of granules of superoxide dismutase and peroxidase, respectively. The lipoxygenase inhibitor, nordihydroguaiaretic acid, completely abolished the enhanced CL of AM preincubated with MCGs and subsequently stimulated by zymosan, but O2- production was not affected by nordihydroguaiaretic acid. Taken together, these results suggest that derivatives of arachidonic acid metabolism, most likely those of the lipoxygenase pathway, are responsible for the enhanced AM CL response observed in the presence of MCGs. Thus, mast cell-macrophage interactions may be important within the airway in enhancing the generation of mediators that contribute to tissue inflammation and bronchospasm.
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PMID:Mast cell granules modulate alveolar macrophage respiratory-burst activity and eicosanoid metabolism. 217 47

The effect of mast cells and mast cell granules on macrophage O2- release as determined by cytochrome c reduction was studied. In vitro activation of mast cells before macrophage activation caused a decrease in O2- -mediated cytochrome c reduction. This decrease was proportional to mast cell activation and reached 80% to 100% when mast cell mediator release was 40% to 50%. Incubation of isolated mast cell granules with macrophages before activation also inhibited O2- -mediated cytochrome c reduction in a dose-dependent manner. Mast cell granule-mediated inhibition of cytochrome c reduction was not caused by histamine, serotonin, or any other dialyzable components but was found to be caused by the scavenging of O2- by mast cell granule-bound superoxide dismutase. Macrophage uptake of sulfur 35-labeled mast cell granules, electron microscopic localization of mast cell granules in the macrophage phagosomes, and the abrogation of mast cell granule effect when the cells were preincubated at 0 degree C indicate that the effect was associated with the adherence or phagocytosis (or both) of mast cell granules. These results suggest that mast cell granules interact with macrophages and that granule superoxide dismutase scavenges O2- generated by the phagocytes.
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PMID:Modulation of macrophage superoxide-induced cytochrome c reduction by mast cells. 254 Dec 13

Benoxaprofen (BXP) is a nonsteroidal anti-inflammatory drug which causes cutaneous phototoxicity. Because the in vivo phototoxicity may involve photosensitized damage to mast cell membranes, the mechanism for photosensitized damage was studied in a single model system, the red blood cell. Oxygen-dependent and oxygen-independent mechanisms for membrane disruption were detected. Oxygen-dependent lysis was not quenched by superoxide dismutase and was quenched only at high sodium azide concentrations. A two-step mechanism is proposed involving initial photodecarboxylation of BXP to form a lipophilic photoproduct which subsequently photosensitizes membrane damage. Human serum albumin at 0.03% totally inhibited BXP-photosensitized lysis.
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PMID:Benoxaprofen photosensitization of cell membrane disruption. 669 24

Cultured rat embryonic skin fibroblasts phagocytosed rat mast cell granules added to the medium or released from co-cultured mast cells by rabbit anti-rat IgE or Compound 48/80. Electron microscopy of fibroblasts incubated with mast cell granules revealed that granules adjacent to the plasmalemma were engulfed by long, thin cytoplasmic processes. Internalization proceeded to fusion of encircling processes and formation of phagosomes. Microtubules and 60 A microfilaments became closely associated with the phagosomal membrane to which small vesicles and cisternae of endoplasmic reticulum fused. The rate of uptake of mast cell granules by fibroblasts was dependent upon temperature and granule concentration. Cytochalasin B inhibited granule uptake whereas colchicine and nocodazole had little effect. Phagocytosis was not influenced by actinomycin D and cycloheximide, was partially inhibited by fluoride, and was markedly inhibited by cyanide, azide, and 2,4-dinitrophenol. Supernatants from fibroblast cultures incubated with mast cell granules for 24 and 48 hr, during which period phagocytosis occurred, contained elevated levels of collagenase and beta-hexosaminidase, but normal levels of lactate dehydrogenase and superoxide dismutase. These results support the concept that immediate hypersensitivity reactions are in part terminated by phagocytosis of biologically active discharged mast cell granules by resident connective tissue fibroblasts. Further, it is suggested that a consequence of this process is an alteration in fibroblast behavior, providing a unique link between immediate hypersensitivity reactions and connective tissue responses to inflammation.
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PMID:Phagocytosis of mast cell granules by cultured fibroblasts. 684 86


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