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PubMed1977

Delayed cold-induced urticaria: a dominantly inherited disorder.

A delayed cutaneous response to cold, characterized by areas of erythematous, edematous deep swelling at 9 to 18 hr after experimental ice challenge, was recognized in a 10-yr-old boy and several members of his family. Biopsy of the cold-induced lesion showed edema and an infiltrate of mononuclear cells; mast cells were normal, and immunoglobulins, complement factors, and fibrin were not detected by immunofluorescence techniques. Local cold challenge did not release histamine or induce alterations in the complement system or the enzymes, histaminase, and histamine methyl transferase. The delayed cutaneous response to cold could not be passively transferred with serum or tissue extracts to monkey skin. Family studies suggested an autosomal-dominant mode of inheritance.

Amine Oxidase (Copper-Containing)↗
PubMed1986

Histamine augments interleukin-2 production and the activation of cytotoxic T lymphocytes.

Histamine (0.5 g/kg) was found to augment the activation of cytotoxic T lymphocytes in vivo, if injected in the late phase (day 4) of the response. The production of interleukin-2 in concanavalin A-activated spleen cell cultures was also strongly augmented by 1 X 10(-2) M histamine or by a combination of 2 X 10(-3) M histamine and histaminase (diamine oxidase). This suggests the possibility that the augmentation in vivo is mediated by the oxidized histamine derivative imidazolylacetaldehyde, since diamine oxidase occurs in many tissues. The interleukin-2-dependent proliferation of a T cell clone, on the other hand, was not affected by histamine with or without diamine oxidase. The experiments suggest that histamine supports the late phase of the cytotoxic T lymphocyte response by augmenting the interleukin-2 production.

Animals↗
PubMed1996

Evidence of semicarbazide-sensitive amine oxidase activity in guinea pig tissues.

Lung, heart tissues and blood plasma of guinea pigs were investigated to see if tissue-bound semicarbazide-sensitive amine oxidase activities with a high affinity for benzylamine (Bz.SSAO) were present in this species as well as in others. This paper shows that these enzymic activities are present in guinea pig lung and heart where they are mainly localized in the cytosol and in microsomal fraction. These activities have a high affinity for benzylamine and appear unable to oxidize histamine at an appreciable rate in agreement with the observation that the purified Bz.SSAO of guinea pig skin shows weak histaminase activity. These guinea pig Bz.SSAO activities show some homology with the pure pig plasma benzylamine oxidase. They crossreact with the antibodies raised in the rabbit against the pig plasma enzyme. Benzylamine oxidase activity was also found in guinea pig blood plasma.

Amine Oxidase (Copper-Containing)↗
PubMed2005

In vivo PAF-induced airway eosinophil accumulation reduces bronchial responsiveness to inhaled histamine.

Chronic eosinophilic bronchitis and bronchial hyperresponsiveness have been considered to be the fundamental features of bronchial asthma. However, the role of airway eosinophils in bronchial responsiveness in vivo has not been fully discussed. The aim of this study was to investigate the direct effect of airway eosinophil accumulation on bronchial responsiveness in vivo. Guinea pigs were transnasally treated with platelet activating factor (PAF) or vehicle twice a week for a total of 3 weeks. Anesthetized guinea pigs were surgically cannulated and artificially ventilated 48 h after the last administration of PAF or vehicle. Ten minutes after the installation of artificial ventilation, ascending doses of histamine were inhaled. In a subsequent study, selective inhibitors of diamine oxidase and histamine N-methyltransferase were intravenously administered before the histamine inhalation in the PAF-treated animals. Next study was conducted 20 min after treatment with indomethacin in this study line. Finally, ascending doses of methacholine were inhaled in our animal model. Proportion of eosinophils and the number of nuclear segmentation in bronchoalveolar lavage fluid significantly increased in guinea pigs treated with PAF compared with vehicle and this finding was confirmed histologically. Nevertheless, bronchial responsiveness to inhaled histamine, but not methacholine, was significantly decreased by the PAF treatment. This bronchoprotective effect induced by PAF remained following aminoguanidine and histamine N-methyltransferase administration, but abolished by treatment of indomethacin. These results suggest that in vivo airway eosinophils may reduce nonspecific bronchial responsiveness through production of inhibitory or bronchoprotective prostanoids, but not through histaminase production.

Administration, Inhalation↗
PubMed1992

Purification of human placenta diamine oxidase.

Diamine oxidase (histaminase) is produced at very high levels by the decidual cells of the placenta. The presence of diamine oxidase has been demonstrated in human neutrophils. Purification of human placenta diamine oxidase was performed by four subfractionation steps and led to the isolation of one polypeptide whose molecular weight was 84,000, as assessed by SDS PAGE. Using polyclonal antibodies raised against the purified enzyme, we have demonstrated that the neutrophil diamine oxidase is immunochemically identical to the placental diamine oxidase. Development of immunological methods will be useful for detection and quantitation of diamine oxidase in neutrophils during the inflammation process.

Amine Oxidase (Copper-Containing)↗
PubMed1999

In vivo airway eosinophil accumulation does not enhance antigen- or propranolol-induced bronchoconstriction in guinea pigs.

BACKGROUND: Chronic airway eosinophil accumulation is characteristic of asthma. However, it remains unclear whether airway eosinophils enhance or reduce release of chemical mediators and/or action of the released mediators in the airways in vivo, because previous investigators have indicated that eosinophil-derived factors such as histaminase and arylsulfatase may alter the allergic reaction by metabolizing chemical mediators. Recently, we have developed a guinea pig model of propranolol-induced bronchoconstriction (PIB), which is mediated by lipid mediators such as thromboxane A2 (TxA2), cysteinyl leukotrienes (cLTs) and platelet activation factor (PAF). This study was conducted to explain the influence of airway eosinophil accumulation on antigen-induced bronchoconstriction and the following PIB, both of which are mediated by lipid mediators. METHODS: Guinea pigs were transnasally treated with 75 microg/kg of polymyxin-B or vehicle twice a week for a total of 3 weeks. Guinea pigs were anesthetized and treated with diphenhydramine hydrochloride, and then artificially ventilated 24 h after the last administration of polymyxin-B or vehicle followed by passive sensitization. Propranolol at a concentration of 10 mg/ml was inhaled 20 min after an aerosolized antigen challenge. RESULTS: The proportion of eosinophils in bronchoalveolar lavage fluid obtained 15 min after the propranolol inhalation was significantly increased in guinea pigs treated with polymyxin-B compared with the vehicle. The polymyxin-B treatment did not affect antigen-induced bronchoconstriction or the following PIB. CONCLUSIONS: We conclude that eosinophils accumulated in the airways by polymyxin-B does not affect release of chemical mediators induced by antigen or propranolol inhalation, or action of released mediators in vivo.

Administration, Inhalation↗
PubMed2000

Role of histamine in allergic conjunctivitis.

Histamine remains the main mediator released by both specific allergic and non-specific mast cell activation. Histamine is the classic mediator of itching, flare and redness. The effects of histamine in allergic conjunctivitis are mediated by H1-receptor activation on blood vessels and nociceptive nerves. Histamine effects may be prolonged and exaggerated since a defect in the histaminase enzymes has been recently demonstrated in VKC. The effects of histamine on conjunctival tissues may be more complex than those manifested by the simple symptom of itching. In fact, proinflammatory effects of histamine on conjunctival epithelial cells and fibroblasts have been demonstrated. Preliminary results showed that the H1 antagonist, emedastine, reduces significantly cytokine production from histamine-stimulated fibroblasts.

Conjunctivitis, Allergic↗
PubMed1983

Catabolism of histamine in the isolated glomeruli and tubules of the rat kidney.

Histamine alters renal hemodynamics including the glomerular microcirculation, and histamine receptors are present in rat glomeruli. We have recently shown that isolated rat glomeruli, but not cortical tubules, incubated with the histamine substrate L-histidine synthesize histamine. This study explores the catabolic pathways of histamine in isolated glomeruli and cortical tubules of the rat kidney. Glomeruli and cortical tubules were incubated with radiolabelled histamine, and the products were separated on thin layer chromatography (TLC). Glomeruli predominantly catabolized histamine to acid metabolites of the diamine oxidase (histaminase) pathway, imidazole acetic acid and ribosylimidazole acetic acid, and to a lesser extent to the inactive methylation product, N tau-methylhistamine (7.5% vs. 2.5%). Tubules on the other hand catabolized histamine to N tau-methylhistamine and to a lesser degree to acid metabolites (7.6% vs. 2.3%). The methyl donor S-Adenosyl-methionine (SAM) (10(-4) M) markedly enhanced the production of N tau-methylhistamine in both glomeruli and tubules (delta + 600%) but had no effect on the production of acid metabolites. In the presence of equimolar concentrations of SAM, tubules continued to methylate histamine to a greater extent than glomeruli (46.0% vs. 18%). In both glomeruli and tubules, the diamine oxidase inhibitor, amino-guanidine, abolished the production of acid metabolites while amodiaquine and pyrilamine, inhibitors of the methylation pathway, markedly reduced the production of N tau-methylhistamine. In addition, in the presence of SAM, tubules catabolized nonlabelled histamine to a greater extent than glomeruli.(ABSTRACT TRUNCATED AT 250 WORDS)

Amine Oxidase (Copper-Containing)↗
PubMed2001

Potentiation by histamine of synaptically mediated excitotoxicity in cultured hippocampal neurones: a possible role for mast cells.

Excessive glutamatergic neurotransmission, particularly when mediated by the N:-methyl-D-aspartate (NMDA) subtype of glutamate receptor, is thought to underlie neuronal death in a number of neurological disorders. Histamine has been reported to potentiate NMDA receptor-mediated events under a variety of conditions. In the present study we have utilized primary hippocampal neurone cultures to investigate the effect of mast cell-derived, as well as exogenously applied, histamine on neurotoxicity evoked by excessive synaptic activity. Exposure of mature cultures for 15 min to an Mg(2+)-free/glycine-containing buffer to trigger synaptic transmission through NMDA receptors, caused a 30-35% neuronal loss over 24 h. When co-cultured with hippocampal neurones, activated mast cells increased excitotoxic injury to 60%, an effect that was abolished in the presence of histaminase. Similarly, addition of histamine during magnesium deprivation produced a concentration-dependent potentiation (+ 60%; EC(50) : 5 microM) of neuronal death which was inhibited by sodium channel blockers and NMDA receptor antagonists, although this effect did not involve known histamine receptors. The histamine effect was further potentiated by acidification of the culture medium. Cultures 'preconditioned' by sublethal (5 min) Mg(2+) deprivation exhibited less neuronal death than controls when exposed to a more severe insult. NMDA receptor activation and the extracellular regulated kinase cascade were required for preconditioning neuroprotection. The finding that histamine potentiates NMDA receptor-mediated excitotoxicity may have important implications for our understanding of conditions where enhanced glutamatergic neurotransmission is observed in conjunction with tissue acidification, such as cerebral ischaemia and epilepsy.

Age Factors↗
PubMed1996

Substrate specificity of lentil seedling amine oxidase.

Copper diamine oxidase from lentil (Lens culinaris) seedlings was shown to be able to catalyze the oxidative deamination of a wide range of aliphatic and aromatic monoamine compounds, including some amino acids. Although the catalytic efficiencies were only 1-3% of that measured with the diamine substrate putrescine, they were still comparable to those of specialized monoamine oxidases. In particular, the lentil enzyme oxidized benzylamine and histamine with K(m) and Vmax values similar to those found for the mammalian enzymes benzylamine oxidase and histaminase. Cysteamine was found to be a substrate of the enzyme, whereas hypotaurine and taurine were found to be neither substrates nor inhibitors of the enzyme. Quite unexpectedly the amino acids L-ornithine and L-lysine were oxidized by lentil enzyme, and beta-alanine and gamma-aminobutyric acid were oxidized only at high concentrations of enzyme. These results suggest that enzymes normally classified as diamine oxidases could in fact have a more diversified role in metabolism than recognized so far.

Amine Oxidase (Copper-Containing)↗
PubMed1975

The selective eosinophil chemotactic activity of histamine.

Histamine diphosphate was shown to selectively attract human eosinophils from mixed granulocyte populations when over 20% eosinophils were used in a modified Boyden chamber chemotactic assay system. This effect of histamine is abolished by incubation with diamine oxidase (histaminase) and was generated by decarboxylation of L-histidine. A linear dose dependent increase in eosinophil migration was observed between 3 X 10(-7) M and 1.25 X 10(-6) M, while higher concentrations of histamine inhibited the migration of eosinophils. The attractant activity of histamine was not inhibited by H-1 or H-2 receptor antagonists, however, the inhibition of migration observed at higher histamine concentrations was reversed by metiamine, an H-2 receptor antagonist. The effects of histamine upon eosinophil migration were demonstrable using three different assays: (a) counting cells that had traversed 5-mum pore, 12-mum thick polycarbonate filters, (b) counting cells that had migrated various distances into a 3-mum pore, 145-mum cellulose nitrate filters, or (c) measuring the number of cells that had traversed an upper polycarbonate filter and migrated into a lower cellulose nitrate filter using 15Cr-labeled cells. The ability of histamine to enhance eosinophil migration was shown to be dependent upon the presence of a concentration gradient; histamine did not cause a dose-dependent increase in random motility. Furthermore, preincubation of the eosinophils with histamine deactivate the cells to further stimulation by histamine or by C5a. It is concluded that in low doses histamine is a chemoattractant for human eosinophils, while in higher doses histamine inhibits eosinophil migration. These observations may relate to the influx and localization of eosinophils in immediate hypersensitivity reactions.

Amine Oxidase (Copper-Containing)↗
PubMed1988

Reversal by ascorbic acid of suppression by endogenous histamine of rat lymphocyte blastogenesis.

Addition of concanavalin A (Con A) to a culture of spleen cells of ODS-od/od rats, which cannot synthesize ascorbic acid, increased the activity of histidine decarboxylase (HDC) in the culture, leading to accumulation of histamine (Hm) in the medium. Treatment of the culture with cimetidine, a type 2 Hm antagonist, enhanced Con A-dependent lymphocyte blastogenesis even in the absence of any exogenously added Hm. Addition of low doses of histaminase increased Con A-dependent lymphocyte transformation. At higher doses, it abrogated the reaction. At concentrations of more than 10(-10) M, exogenously added Hm suppressed the Con A-dependent uptake of [3H]thymidine by the lymphocytes, but it significantly augmented the response at 10(-14) M. The addition of ascorbic acid (10(-8)-10(-5) M) to the culture suppressed the Con A-mediated HDC induction and inhibited Hm biosynthesis. Concomitantly added ascorbic acid at the concentrations of 10(-8)-10(-4) M increased the uptake of [3H]thymidine dependent on Con A or phytohemagglutinin by the lymphocytes. These results suggest that mitogen-dependent lymphocyte blastogenesis is activated by Hm produced by the spleen cells per se. However, when culture was prolonged, high concentrations of Hm suppressed the reaction. Ascorbic acid enhances mitogen-dependent lymphocyte blastogenesis through inhibition of HDC induction, leading to attenuation of immunosuppressive Hm production by the spleen cells.

Animals↗
PubMed1989

Kinetic studies on the inhibition mechanism of diamine oxidase from porcine kidney by aminoguanidine.

The mechanism of inhibition of diamine oxidase [DAO, histaminase, amine: oxygen oxidoreductase (deaminating) (copper-containing), EC 1.4.3.6] by aminoguanidine was studied kinetically. The DAO reaction was carried out with putrescine as a substrate in the presence of o-aminobenzaldehyde and followed by the continuous increase in A430. An enzymatic reaction product, 4-aminobutyraldehyde, was spontaneously cyclized to delta 1-pyrroline, which coupled with o-aminobenzaldehyde to give rise to a yellow quinazolinium chromophore [Holmstedt et al. (1961) Biochim. Biophys. Acta 48, 182-186]. First, to measure the initial velocities as accurately as possible, the kinetic relationship between the oxidase reaction rate and the color development rate was formulated. The reaction proceeded linearly in the absence of aminoguanidine, but slowed down time-dependently in its presence. When the color development velocities in the presence of the inhibitor were plotted against time, the plot was nonlinear and there seemed to be at least two phases of the inhibition. Nonlinear least-squares analysis of the data dA430/dt showed that the simplest model that fitted best was a model composed of two species of enzyme-inhibitor complexes: E + I k+1 in equilibrium k-1 EI k+2 in equilibrium k-2 E'I where E is the enzyme, I is aminoguanidine (an inhibitor), and the ks are the rate constants.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehydes↗
PubMed1978

Studies on the formation of gamma-aminobutyric acid from putrescine in rat organs and purification of its synthetic enzyme from rat intestine.

The formation of gamma-aminobutyric acid (GABA) from putrescine was examined in organs of rats using radioactive putrescine. Radioactive GABA was detected in all the organs of a rat injected intraperitoneally with radioactive putrescine, and the highest radioactivity of GABA was observed in the small intestine. The enzyme involved in this formation was purified from small intestine and identified as a diamine oxidase, histaminase, from the properties of the enzyme. Activity of the enzyme was found in all the organs of rat, and the highest activity was observed in the small intestine.

Amine Oxidase (Copper-Containing)↗
PubMed1999

Isoniazid drug and food interactions.

Isoniazid inhibits the metabolism of several drugs, resulting in clinically significant interactions in some patients. Clinical trials and case reports have documented that isoniazid can cause increased phenytoin and carbamazepine serum concentrations and toxicity. In relatively high doses, isoniazid can also cause increased effect of theophylline and warfarin. Isoniazid inhibits metabolism of selected benzodiazepines and vitamin D. Inhibition of monoamine oxidase and histaminase by isoniazid can cause significant drug-food interactions. Food greatly decreases isoniazid bioavailability. Although probably best recognized as an inhibitor of drug metabolism, isoniazid has a biphasic effect of inhibition-induction on one cytochrome P450 isozyme, CYP2E1, which partially explains the interaction with acetaminophen and increased risk of hepatotoxicity. Continued investigations will likely result in discovery of new isoniazid interactions.

Antitubercular Agents↗
PubMed1985

Isoniazid interactions.

Isoniazid is an antituberculous drug that is usually administered for nine to 12 months. The potential for clinically important interactions exists because this drug is a potent inhibitor of drug metabolism. Studies and case reports have shown that isoniazid inhibits the metabolism of several drugs, including phenytoin, carbamazepine, anticoagulants, benzodiazepines, and vitamin D. Furthermore, isoniazid inhibits both monoamine oxidase and diamine oxidase (histaminase). Additional study is required to document the clinical significance of other isoniazid interactions. Future investigations will identify new isoniazid interactions.

Animals↗
PubMed1990

Recurrent urticaria and reduced diamine oxidase activity.

An abnormal metabolism of histamine has been suspected in urticaria and the role of diamine oxidase (DAO: histaminase) is therefore of interest. We have studied DAO activity in plasma and jejunal biopsy material and have measured the post-heparin DAO release in 11 control subjects and nine with recurrent urticaria, three of whom had had concurrent episodes of abdominal pain. Two of the nine urticaria subjects had only a minimal rise in plasma DAO activity after heparin, three had a response which was at the lower end of the normal range, and four were normal. In four out of five cases in which jejunal biopsy activity was obtained, there was concordance between mucosal DAO activity and the post-heparin plasma DAO response. Those with abdominal symptoms had abnormally low mucosal DAO activity and the subject who was most severely affected had proven episodes of small bowel oedema.

Adult↗
PubMedDate not supplied

The effects of imidazole on contractility and cyclic AMP levels of guinea-pig tracheal smooth muscle.

1. Imidazole contracted guinea-pig isolated tracheal smooth muscle, and at low concentrations (50 mumol/l to 2 mmol/l) also enhanced contractions induced by histamine. 2. Imidazole had no effect on contractile responses to potassium chloride, acetylcholine, prostaglandin F2 alpha, or the ionophore A23187; nor did it affect anaphylactic contractions in tracheal strips from guniea-pigs sensitized to ovalbumin. 3. Imidazole had no effect on the content on cyclic AMP in guinea-pig tracheal smooth muscle, nor did it affect the accumulation of cyclic AMP induced by histamine, isoprenaline, theophylline plus isoprenaline, or prostaglandin E1. 4. Imidazole-induced contractions were partially antagonized by atropine, mepyramine maleate and the omission of extracellular calcium ions. 5. Imidazole-induced hyperreactivity to histamine was not affected by atropine or indomethacin, and was more pronounced in the absence of extracellular calcium ions. 6. It is concluded that imidazole does not affect cyclic nucleotide phosphodiesterase activity in guinea-pig trachea, and its effects on contractile responses of the smooth muscle are unrelated to any action of cyclic AMP metabolism. The potentiating effect of imidazole may involve inhibition of histaminase, or the facilitation of calcium ion release from intracellular storage sites.

Animals↗