Xanthine oxidase-induced histamine release from isolated rat peritoneal mast cells: involvement of hydrogen peroxide

Ohmori, Hitoshi; Komoriya, Keiji; Azuma, Akiko; Kurozumi, Seizi; Hashimoto, Yoshiro

doi:10.1016/0006-2952(79)90524-0

Cited by 80 publications

(33 citation statements)

References 12 publications

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“…Histamine may be released from these cells either through a selective, noncytotoxic exocytosis of stored granules, or through a nonselective (cytotoxic) altera tion of the plasma membrane. In vitro stud ies indicate that free radicals may play a role in activating both of these mechanisms [5,24,25]. The present study demonstrates that this may also be the case under in vivo con ditions after intestinal ischemia.…”

Section: Discussionsupporting

confidence: 71%

Oxygen Free Radical-Induced Histamine Release during Intestinal Ischemia and Reperfusion

1989

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Acute mesenteric ischemia is highly lethal and therefore a serious problem for surgery and intensive care medicine; accordingly its pathophysiology warrants further study. Oxygen free radicals (OFR) play a role in the intestinal mucosal damage that develops during reperfusion after ischemia. Histamine (H) is generally released in various types of tissue ischemia. The link between H release and OFR has only been studied in in vitro systems. We tested the hypothesis that OFR may be involved in H release following reperfusion of the ischemic gut. The artery supplying a segment of the ileum was occluded for 1 or 2 h in anesthetized dogs. On reperfusion, a release of H into the venous effluent of the segment was demonstrated. Pretreatment of the animals with allopurinol (an inhibitor of xanthine oxidase), or with MTDQ-DA [6,6’-methylenebis(2,2-dimethyl-4-methanesulfonic acid sodium-1,2-dihydroquinoline)], a superoxide anion scavenger, or with a combination of allopurinol and MTDQ-DA resulted in an inhibition of H release. We conclude that OFR may play a role in the local H release following intestinal ischemia.

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Section: Discussionsupporting

confidence: 71%

Oxygen Free Radical-Induced Histamine Release during Intestinal Ischemia and Reperfusion

1989

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“…For example, chemically derived superoxide, generated from xanthine-xanthine oxidase (15,44,45) or potassium superoxide (46), and hydrogen peroxide (47) have been shown to induce rat peritoneal mast cell degranulation. Furthermore, FMLP-(48) or zymosan-activated (49) human neutrophils at high cell density (10 6 /ml) caused mast cell histamine release, and the oxidant responsible was identified as hydrogen peroxide.…”

Section: Discussionmentioning

confidence: 99%

A Comparison of Reactive Oxygen Species Generation by Rat Peritoneal Macrophages and Mast Cells Using the Highly Sensitive Real-Time Chemiluminescent Probe Pholasin: Inhibition of Antigen-Induced Mast Cell Degranulation by Macrophage-Derived Hydrogen Peroxide

Swindle

Hunt

Coleman

2002

The Journal of Immunology

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Mast cells and macrophages live in close proximity in vivo and reciprocally regulate one another’s function in various ways. Although activated macrophages possess a powerful reactive oxygen species (ROS) generating system, there is conflicting evidence regarding whether mast cells can produce ROS. We used the highly sensitive real-time chemiluminescent probe Pholasin to examine ROS release by peritoneal macrophages and mast cells isolated from OVA-sensitized rats. Macrophages stimulated with PMA (0.8 μM) or ionomycin (1 μM), but not OVA (1 μg/ml), released high-level ROS, levels of which peaked after 3–7 min and declined to baseline levels within 1 h. Superoxide was identified as the major ROS species induced by PMA but not by ionomycin. In contrast, purified mast cells stimulated with PMA released low-level ROS, which was entirely due to the contaminating (2%) macrophages, and did not release any detectable ROS in response to ionomycin or OVA at concentrations that induced degranulation. Stimulation of mixed cell populations with PMA to induce macrophage ROS release led to 50% inhibition of serotonin release from mast cells stimulated 5 min later with OVA. The PMA-induced inhibitory factor was identified as hydrogen peroxide. In conclusion, activated rat peritoneal macrophages but not mast cells produce ROS, and macrophage-derived hydrogen peroxide inhibits mast cell degranulation. The latter could be an important mechanism whereby phagocytic cells regulate mast cell activation and promote resolution of IgE-mediated inflammation.

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“…During this period, sperm produce large amounts of H202 (1) which by itself has been found to stimulate in vitro many of the biochemical consequences of capacitation (I. Bize et al, manuscript in preparation). Likewise, small amounts of H202 are known to trigger the process of histamine secretion by mast cells, suggesting the oxidant may also play a role in initiating the inflammatory response (32). Since the interaction of several hormones with their receptors has been found to regulate transplasma membrane redox enzymes capable of oxidizing NADH to generate H202…”

Section: Discussionmentioning

confidence: 99%

Rapid Stimulation of an Oxidative Burst during Elicitation of Cultured Plant Cells

Apostoł¹,

Heinstein²,

Low³

1989

Plant Physiol.

632

295

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Stimulation of cultured plant cells with elicitors of the defense response leads to the rapid destruction of a variety of watersoluble compounds including indoleacetic acid and certain fluorescent dyes. This destructive activity, which is often vigorously manifested within 5 minutes of elicitor addition, is shown to derive from the rapid production of H202 and its use by extracellular peroxidases. Because of its speed of appearance, this oxidafive burst may qualify as the first induced line of defense against invading pathogens. Since H202 has been implicated as a second messenger of hormone-stimulated metabolic changes in some animal cells, its possible role in transduction of the defense signal in plants was also examined. Not only did exogenous H202 alone stimulate phytoalexin production in the plant cell suspension, but inhibition of elicitor-stimulated phytoalexin production was observed upon addition of catalase and other inhibitors of the oxidative burst. Furthermore, for inhibition to occur, the presence of catalase was required during elicitor addition, since if introduction of the enzyme was delayed until 1 hour after addition of the elicitor, no inhibition resulted. These results suggest that H202 also plays an important role in inducing subsequent defense responses such as phytoalexin production.

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Xanthine oxidase-induced histamine release from isolated rat peritoneal mast cells: involvement of hydrogen peroxide

Cited by 80 publications

References 12 publications

Oxygen Free Radical-Induced Histamine Release during Intestinal Ischemia and Reperfusion

Oxygen Free Radical-Induced Histamine Release during Intestinal Ischemia and Reperfusion

A Comparison of Reactive Oxygen Species Generation by Rat Peritoneal Macrophages and Mast Cells Using the Highly Sensitive Real-Time Chemiluminescent Probe Pholasin: Inhibition of Antigen-Induced Mast Cell Degranulation by Macrophage-Derived Hydrogen Peroxide

Rapid Stimulation of an Oxidative Burst during Elicitation of Cultured Plant Cells

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