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PubMed1957

The oxidation of cystamine and homocystamine by mammalian enzymes.

The oxidative deamination of cystamine and homocystamine by mammalian oxidases has been studied. The histaminase of pig kidney oxidizes homocystamine much more slowly than cystamine. The amine oxidase of mammalian liver (guinea-pig, rabbit) oxidizes homocystamine more rapidly than cystamine. Both amines are oxidized by plasma (or serum) of ruminants (ox, sheep, goat) and of the horse. In the enzymatic oxidation of homocystamine both aminogroups are removed; there is no evidence that a ring compound analogous to cystaldimine is accumulating.

Amine Oxidase (Copper-Containing)↗
PubMed1958

The renal removal of injected [14C] histamine from the blood in dogs.

The amounts of [(14)C]histamine in arterial blood, in renal venous blood and in urine during a steady intravenous infusion of [(14)C]histamine were measured in five anaesthetized dogs. The extraction ratio for [(14)C]histamine was 0.7 to 0.8, indicating that the histamine was efficiently taken up from the blood by the kidney. Only a small part (14 to 18%) of the [(14)C]histamine removed from the blood by the kidney appeared in the urine as histamine. Evidence was obtained that [(14)C]histamine was metabolized in the kidney not only by histaminase (diamine oxidase) but also by the histamine methylating enzyme.

Amine Oxidase (Copper-Containing)↗
PubMed1958

Metabolism of injected [14C] histamine in the kidney of the dog.

In experiments on anaesthetized dogs, [(14)C]histamine was given in a steady infusion into one of the renal arteries, while urine was collected from both kidneys separately. The kidney which received the intra-arterial injection of [(14)C]histamine excreted several times more [(14)C]-labelled methylhistamine, methylimidazoleacetic acid and imidazoleacetic acid than did the other kidney, indicating that histamine may be inactivated in the canine kidney not only by histaminase but also by the histamine methylating enzyme.

Amine Oxidase (Copper-Containing)↗
PubMed1961

Antihistaminase activity of serpentine.

Serpentine, an alkaloid of Rauwolfia serpentina, specifically potentiates histamine responses of guinea-pig ileum, uterus, and tracheal chain. It also inhibits histaminase in vitro. Its antihistaminase activity is equivalent to that of aminoguanidine.

Alkaloids↗
PubMed1961

Some effects of corticosteroids on the metabolism of histamine and 5-hydroxytryptamine in the rat.

Daily intramuscular injections of cortisone, prednisolone, triamcinolone, fludrocortisone and 2-methylfludrocortisone reduced the histidine decarboxylase activity of the rat liver, but increased the enzyme activity of the pyloric stomach. Injections of histamine liberators or exposure to cold produced similar changes. After adrenalectomy, the histidine decarboxylase activities of the liver and pyloric stomach were unaltered, but the histaminase activity of the ileum was reduced. The 5-hydroxytryptophan decarboxylase activities of rat liver and kidney were not altered by treatment with corticosteroids.

Adrenal Cortex Hormones↗
PubMed1961

Effect of thyroid hormones on histamine formation in the rat.

Treatment with thyroxine or liothyronine increased the urinary excretion of free histamine in male and female rats under the influence of aminoguanidine, a histaminase inhibitor. There was no evidence for an altered catabolism of histamine in rats treated with liothyronine, since the same percentage of subcutaneously injected [(14)C]-histamine appeared unchanged in the urine. After subcutaneous injection of [(14)C]-L-histidine, rats treated with liothyronine excreted more [(14)C]-histamine than control rats. An increased formation of [(14)C]-histamine from [(14)C]-histidine could also be demonstrated in vitro, in the glandular portion of the stomach, while no increase was found in the skin.

Amine Oxidase (Copper-Containing)↗
PubMed1974

Drug-induced changes in capillary filtration coefficient and blood flow in the innervated small intestine of the anaesthetized cat.

1 A modification of the Folkow Technique for simultaneous measurement of blood flow and capillary filtration coefficient (CFC) in the cat jejunum is described. The modification retained the sympathetic innervation of the preparation, and in the present experiments, drugs were administered intravenously.2 There is evidence that CFC is a cardiovascular quantity independent of blood flow or regional vascular resistance in these preparations. Low doses of drugs may affect CFC without altering the blood pressure, blood flow, or heart rate.3 Under control conditions the CFC, a measure of functional exchange vessel area, was lower than previously reported for similar, but denervated preparations.4 alpha-Adrenoceptor stimulation with phenylephrine (1.0 mug kg(-1) min(-1), i.v.) caused a fall of 75-85% from control values of CFC with concomitant rises in blood pressure of 0-15% and falls in blood flow of 10-40%. The heart rate rose by 0-15%. Phentolamine (0.5-2.0 mg/kg, i.v.) caused a rise in CFC and a slight fall in vascular resistance, and blocked the effects of phenylephrine on this tissue.5 beta-Adrenoceptor stimulation with isoprenaline (0.2 mug kg(-1) min(-1), i.v.) caused a rise in CFC of 75-110%, a fall in blood pressure of 0-10%, a rise in blood flow of 10-60% and a rise in heart rate of up to 35%. Propranolol caused a transient rise in CFC when injected i.v. in a dose of 0.1 mg/kg, which was adequate to block the effects of isoprenaline.6 Angiotensin (25-100 ng kg(-1) min(-1), i.v.) caused falls in CFC of up to 100% and rises in vascular resistance. Aminophylline (0.2-0.4 mg kg(-1) min(-1), i.v.) caused rises in CFC of up to 200% with falls in vascular resistance.7 Histamine (0.01 to 1.0 mug kg(-1) min(-1), i.v.) had little effect on vascular resistance, but 10 and 40 mug kg(-1) min(-1) caused falls in vascular resistance. Doses up to and including 10 mug kg(-1) min(-1) caused falls in CFC, but the higher doses, or smaller doses after histaminase inhibition caused rises in CFC. alpha-Adrenoceptor blockade reversed the fall in CFC caused by small doses of histamine, to a rise. Mepyramine completely blocked the effects of histamine on these preparations.8 5-Hydroxytryptamine (33-100 mug kg(-1) min(-1), i.v.) caused a rise in vascular resistance and a fall in CFC of up to 85%. These effects were blocked by methysergide (250 mug/kg, i.v.).9 Rises in CFC indicate an increase in functional exchange vessel area in the tissue, and falls in CFC a decrease in the area available for vascular exchange. These changes are examined against the possibility of the drugs causing reflex adjustments in sympathetic tone, of systemic deactivation of intravenously administered drugs, and of drug effects on vascular permeability.

Aminophylline↗
PubMed1997

Some histamine-related compounds interacting with the benzylamine-oxidizing activity of rat white adipocytes.

In rat white adipocytes histamine is oxidized by a semicarbazide-sensitive amine oxidase which has benzylamine or preferential substrate (Bz-SSAO). To determine whether Bz-SSAO could control the extracellular levels of histamine and other histamine-related compounds active in lipid mobilization, a series of histaminergic compounds was screened as possible substrates or inhibitors of Bz-SSAO activity. Histaminergic compounds with imidazolo or thiazolo groups are oxidized by rat white-adipocyte Bz-SSAO whereas S-isothiourea derivatives, with two- or three-carbon-atom alkyl chains between the isothiourea and the N,N-dimethyl residue are, instead, inhibitors of the enzyme. Amtamine has been identified as a selective, high affinity substrate for rat white adipocyte Bz-SSAO. This enzymatic degradation might represent a catabolic pathway for the drug. These results show that the histaminase property of the rat white-adipocyte enzyme Bz-SSAO also extends to other histamine derivatives active at histamine receptors.

Adipocytes↗
PubMed1975

Effect of ascorbic acid on histamine metabolism in scorbutic guinea-pigs.

1. In guinea-pigs fed an ascorbic-acid-free diet, as the ascorbic acid levels decreased the histamine levels in blood and urine rose steadily to maxima in about 10-12 days. The elevated histamine levels persisted in the blood and urine of scorbutic guinea-pigs and the histamine levels in lung, gastric mucosa and spleen also increased. The increased histamine content of the urine, blood and other tissues in the ascorbic-acid-depleted condition could be brought back to normal levels by administration of a single dose of ascorbic acid 5 mg/100 g body wt. guinea-pig. 3. The drop in the elevated histamine level was not due to an indirect effect of ascorbic acid on histamine forming capacity, histaminase activity or histamine release.

Amine Oxidase (Copper-Containing)↗
PubMed1990

Raised histamine concentrations in chronic cholestatic liver disease.

Pruritus is a frequent symptom in chronic cholestatic liver disease. To date, no single causative mechanism has been identified. We examined venous plasma concentrations of the known pruritogen, histamine, using a highly sensitive radioenzymatic assay in 42 patients with chronic cholestatic liver disease, and in normal controls. The mean plasma histamine level was significantly greater in chronic cholestatic liver disease patients (275 (117) pg/ml; X (SD) than in controls (140 (72) pg/ml, n = 20) (p less than 0.0001). No significant differences were found between histamine concentrations in the two chronic cholestatic liver disease subgroups: primary biliary cirrhosis and sclerosing cholangitis. Histamine concentrations were significantly greater (p less than 0.01) in the pruritic (319 (132) pg/ml) as compared with the non-pruritic (227 (75) pg/ml) chronic cholestatic liver disease patients. The histaminase activity was equivalent in patients and controls. The finding of raised histamine concentrations in chronic cholestatic liver disease suggests in vivo mast cell activation and a potential role for its mediators in the pruritus characteristic of these disorders.

Adult↗
PubMed1984

Role of histamine in the aetiology of byssinosis. II. Lung histamine concentrations in guinea pigs chronically exposed to cotton and flax dusts.

Data presented in this study support the finding that cotton and flax dusts contain agents which potentiate the formation or accumulation of histamine or both in the lungs of guinea pigs exposed to dust, and that such agents are present at much higher levels in cotton dust than in flax dust. The potentiating effect may be through the recruitment of mast cells into the lung. Both cotton and flax dusts contain methylating enzyme inhibitory agents, whereas cotton dust also contains agents that inhibit histaminase activity; flax dust contains agents potentiating histamine activity. These agents working together result in the accumulation or depletion of histamine observed in the different groups of animals exposed to either cotton or flax dust in this study.

Animals↗
PubMed1992

Diamine oxidase activity in the duodenal mucosa of rats with cysteamine-induced ulceration.

Cysteamine administration to rats is followed by a high incidence of duodenal ulceration. The effect of cysteamine on the activity of diamine oxidase (DAO, histaminase) in the duodenal mucosa of the rat was investigated. Rats were injected subcutaneously with cysteamine on 2 successive days at doses of 10, 20 and 40 mg/100 g body weight and killed 24 h after the second dose. The results indicated that cysteamine at a dose of 40 mg/100 g body weight inhibited enzyme activity by about 27% (p less than 0.05). Lower doses of cysteamine did not significantly affect enzyme activity. In another experiment, rats were injected subcutaneously with either saline (control) or cysteamine at a single dose of 40 mg/100 g body weight and killed 4, 8, 12, 24, 48 and 60 h thereafter. The ulcerogen produced progressive reductions in enzyme activity, which were significant at 12 h (22% reduction) and 24 h (25% reduction). At 60 h, enzyme activity was not significantly different from that of control.

Amine Oxidase (Copper-Containing)↗
PubMedDate not supplied

Diamine oxidase: an overview of historical, biochemical and functional aspects.

This article is a review of the historical, biochemical, and functional aspects of the enzyme diamine oxidase (DAO). The amine oxidase DAO, formerly called histaminase, is found in various tissues, but is especially active in the intestinal mucosa. Its function is the oxidative deaminating of several polyamines, essential substances for cell proliferation. DAO is thus a regulating enzyme in rapidly proliferating tissues such a bone marrow and intestinal mucosa. Results from several studies have demonstrated that both ornithine decarboxylase (ODC) and DAO activity rise during adaptive hyperplasia seen after small bowel resection. The ODC-dependent increase in polyamine content and subsequent increase in cell proliferative activity is probably downregulated locally in the villus tip by the increased DAO activity. DAO is normally present in very small amounts in the circulation and its basal plasma levels are positively correlated with the maturity and integrity of the intestinal mucosa. After intravenous administration of heparin, DAO is released from its capillary binding sites in the lamina propria into the peripheral circulation. Measurement of postheparin DAO release enhances its sensitivity and is now extensively studied to assess its value as follow-up or screening test for several enteropathies. Measuring basal as well as postheparin DAO levels has potential relevance following small bowel transplantation. Rejection of the small bowel graft leads to mucosal damage, which could conceivably lead to changes in DAO activity.

Amine Oxidase (Copper-Containing)↗
PubMed1990

Endogenous histamine in immune inflammation in 6-day-old air pouch of facsimile synovium.

Immune inflammation was induced by injecting bovine serum albumin (BSA) into 6-day-old air pouches of mice presensitized with 2 weekly injections of an emulsion containing BSA and complete Freund's adjuvant. Control mice were also similarly pretreated with the same emulsion without BSA. The results show that the numbers of exudate leucocytes in the air pouches of both test and control groups increased and peaked at 4 h and then declined after the antigen challenge. However, the values of exudate leucocytes in the test animals at 4- and 24-hour intervals were significantly lower than those of the control. On the other hand, exudate histamine of the test group peaked at 1 h, and this was significantly higher than that of the control. Injection of exogenous histamine or histaminase with the challenging antigen increased the number of exudate leucocytes in both test and control animals. The findings thus suggest that endogenous histamine released in immune inflammation most probably plays the same role as in non-immune inflammation by enhancing the vascular permeability at the inflammatory site in the early phase of the inflammatory reaction.

Animals↗
PubMed1992

Role of histamine in the chemotactic deactivation of polymorphonuclear leukocytes following incubation with formylmethionyl peptides.

To clarify the mechanism of chemotactic deactivation of polymorphonuclear neutrophils (PMN) following incubation with the synthetic dipeptide N-formylmethionyl phenylalanine (FMP), we tested the hypothesis that histamine, which is released from leukocytes during incubation with FMP, could explain this inhibition. Human PMN were incubated in the presence or absence of FMP (10(-7) to 10(-5) M) and histamine measured fluorometrically in the supernatant. Washed PMN were then tested in Boyden chambers against FMP (10(-5) M) and other chemoattractants. Incubation of leukocytes with FMP caused a nonpreferential PMN deactivation which was proportionally and kinetically related to FMP-induced histamine release. No histamine release or chemotactic deactivation was observed in the absence of Ca2+ and Mg2+. The inhibitory effect of the peptide was significantly prevented by an H2 blocker or when using basophil-depleted PMN suspensions. Histaminase abolished the capacity of FMP-incubated leukocyte supernatants to decrease PMN chemotaxis. Preincubation of leukocytes with anti-IgE or a sensitizing allergen caused a significant PMN chemotactic deactivation. These results show that histamine which is released during leukocyte incubation with FMP, contributes, at least in part, to the chemotactic deactivation of PMN.

Amine Oxidase (Copper-Containing)↗
PubMed1996

Ultrastructural detection of histamine in human mast cells developing from cord blood cells cultured with human or murine recombinant c-kit ligands.

Immature human mast cells, arising from cord blood mononuclear cells cultured in the presence of the c-kit ligand of human or murine origin, contain mixtures of morphologically immature and mature secretory granules. Use of a new cytochemical technique to localize histamine in ultrastructural samples (based on the affinity of the enzyme, histaminase, for its substrate, histamine) localized this amine to mature mast cell granules of all substructural patterns present, as well as to condensation foci appearing in immature cytoplasmic granules. This cytochemical evidence of histamine bound to condensation foci during granule building in developing mast cells is analogous to evidence obtained during granule recovery of degranulated human basophils and mast cells.

Animals↗
PubMed1976

Serotonin vascular reactivity and other clinical pharmacological investigations in two intestinal carcinoid patients.

In two patients with carcinoid syndrome, a reduced venoreactivity to serotonin (5-HT) was found by means of the venoconstriction test. Parachlorophenylalanine (PCPA) treatment increased 5-HT venoreactivity. A normal noradrenaline venoreactivity was detected before and during PCPA administration. The altered platelet monoamine oxidase (MAO) activity corrected by PCPA treatment. The abnormal 5-HT turnover may alter the synthesis of MAO and provoke the production of isoenzymes. Low plasma amine oxidase and high plasma histaminase activity were found in 1 of these 2 patients. A low level of plasma prekallikrein in the two patients remained unchanged during PCPA administration.

Amine Oxidase (Copper-Containing)↗