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PubMed1976

The effect of histamine, isoproterenol and tyramine on rat uterine cyclic AMP.

Isoproterenol (10(-4) M), histamine (10(-3) M) and tyramine (10(-3) M) elevated cyclic AMP levels in incubated rat urerine segments. Promethazine (10(-6) M) an H1-receptor antagonist was ineffective in blocking the increase in cyclic AMP due to isoproterenol, histamine and tyramine. Buriamide (10(-6) M), an H2 receptor antagonist, was effective in almost abolishing the cyclic AMP elevation due to histamine, whereas burimamide did not affect the cyclic AMP levels elevated by tyramine and only slightly reduced the isoproterenol response. Propranolol was effective in reducing or abolishing the cyclic AMP accumulation by all three agonists. The respective blockade by burimamide or propranolol was overcome by increasing the concentration of the agonists. Histamine (10(-3) M) and tyramine (10(-3) M) failed to elevate cyclic AMP in uterine segments obtained from reserpine treated rats. The data supports the hypothesis that histamine, like tyramine, has an indirect effect on the rat uterus mediated through the release of endogenous norepinephrine.

Animals↗
PubMed1991

[Histamine and tyramine levels in selected food products].

Histamine and tyramine contents were determined in parallel in fish and fish products ripening and processed cheese, yeast, wine, cabbage and sauerkraut, and tomato paste. Histamine was assayed by the colorimetric method of Hardy and Smith, and by TLC. Tyramine was determined by TLC. Levels of histamine and tyramine were found to be low in all products tested. For histamine and tyramine, respectively, they amounted: in raw fish to 0.0-8.0 and 0.0-2.6 mg/100 g, in fish products to 0.0-16.0 and 0.0-10.0 mg/100 g, and in cheeses to 0.0-0.8 and 1.3-20.0 mg/100 g. In the remaining food products (tomato paste, yeast, wine, cabbage and sauerkraut), histamine content was between 0.0-16.6 mg/100 g (highest in tomato paste), and tyramine content fluctuated between 0.0-8.0 mg/100 g (highest in sauerkraut).

Animals↗
PubMedDate not supplied

[The comparative influence of pyrazidol, inkazan and other antidepressant monoamine oxidase inhibitors on the pressor effect of tyramine].

In experiments on conscious normotensive male Wistar rats the new antidepressants, reversible MAO-A inhibitors, pyrazidole and incazane, as well as moclobemid increased the pressor effect of orally administered tyramine. The drugs potentiated also the pressor effect of intravenous tyramine. More prolonged potentiation of tyramine action was produced by moclobemid, less prolonged by incazane. The potentiation by the studied MAO-A inhibitors of the pressor effect of tyramine reflects the inhibition of the activity of MAO-A and the first-pass metabolism of tyramine in the gut and liver, as well as the inhibition of intraneuronal MAO activity in noradrenergic nerve endings and the potentiation of sympathetic activity.

Animals↗
PubMed1988

Blood pressure response to tyramine-enriched meal before and during MAO-inhibition in man: influence of dosage regimen.

In an open study oral tyramine in variable doses was administered to six healthy volunteers under three different conditions: 1) without moclobemide, 2) under moclobemide steady-state conditions (3 X 200 mg moclobemide daily) one hour after moclobemide intake and 3) under moclobemide steady-state conditions simultaneously with moclobemide. It was shown that the amount of tyramine effecting 30-50 mmHg systolic blood pressure increase was roughly doubled when moclobemide was administered together with tyramine instead of one hour before tyramine intake. The time interval between tyramine ingestion and maximal blood pressure increase did not differ significantly between conditions 2) and 3). The conclusion of this study is that moclobemide should always be taken at the end of a meal, which is anyway the usual time for drug intake.

Administration, Oral↗
PubMed1986

Dietary tyramine and other pressor amines in MAOI regimens: a review.

A critical review of the literature on amine composition and relevant case reports provides rational guidelines for diet planning and counseling of patients on monoamine oxidase inhibitor (MAOI) drug regimens. Small amounts of normally harmless pressor amines in foods can lead to a hypertensive crisis, which is often termed the "cheese reaction." Initial recognition of the problem led to reduced usage of MAOIs and overzealous food restrictions. Recently, confidence in handling such reactions and in MAOI usage has increased. MAOIs treat anxiety and depression by supposedly inhibiting the inactivation of neurotransmitters. A side effect is the concurrent failure to inactivate the potent vasopressor amine, tyramine. Consumption of 6 mg of tyramine may produce a mild crisis whereas 10 to 25 mg may produce severe headaches with intracranial hemorrhage and its sequelae. Any food rich in aromatic amino acids can become high in tyramine if aging, contamination, prolonged storage, or spoilage occurs. Tables are presented listing the current MAOI drugs; the pressor amines; the tyramine content of various cheeses; and foods to avoid, foods to use with caution, and foods that are not restricted. Rational guidelines for dietary counseling in MAOI usage include: keep tyramine intake below 5 mg, begin diet counseling before drug therapy, monitor patient compliance, recommend preparation and consumption of only fresh foods, and continue the diet four weeks beyond drug therapy.

Diet↗
PubMed1986

[Effect of tyramine on the spinal cord afferent link of pressor reflexes].

In anesthetized cats, tyramine application on the dorsal surface of C6-TI spinal cord segments suppressed the pressor components of blood pressure reflexes evoked by radial nerve A sigma or A + C afferent stimulation. Tyramine application on L4-SI spinal cord segments suppressed pressor reflexes to tibial nerve stimulation. Both the degree and the rate of reflex suppression increased with the rise in tyramine concentration from I to 4%. Along with these local effects "distant" tyramine action was demonstrated: pressor reflexes to radial nerve stimulation increased when tyramine was applied on L4-SI segments, but after its application on C6-TI segments pressor reflexes to tibial nerve stimulation increased in some cats, decreased in the other ones, or remained practically unchanged.

Afferent Pathways↗
PubMed1984

Presence of 1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acids and tyramine as precursors of mutagens in soya sauce after nitrite treatment.

Soya sauce showed marked direct-acting mutagenicity toward Salmonella typhimurium TA 100 after nitrite treatment. Three precursors showing mutagenicity after nitrite treatment were isolated from soya sauce. Their structures were determined to be (-)-(1S,3S)-1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid [(-)-(1S,3S)-MTCA], its stereoisomer (-)-(1R,3S)-MTCA and tyramine. The numbers of revertants of TA 100 induced by 1 mg each of (-)-(1S,3S)-MTCA, (-)-(1R,3S)-MTCA and tyramine, after nitrite treatment, were 17 400, 13 000 and 3 900, respectively, without S9 mix. The amounts of MTCA isomers and tyramine in various Japanese soya sauces showing mutagenicity after nitrite treatment were 82-678 and 17-2 250 micrograms/mL, respectively. Most soya sauces produced in the USA showed weaker mutagenicity than those produced in Japan and contained lower, if not undetectable, amounts of the three precursors of mutagens. The mutagenicity of MTCA isomers and tyramine accounted for 16-61 and 1-35%, respectively, of the mutagenicity of the soya sauces after nitrite treatment. The mutagen(s) produced from (-)-(1S,3S)-MTCA with nitrite was a minor product(s), the major product being the non-mutagen, (-)-(1S,3S)-1-methyl-2-nitroso-1,2,3,4-tetrahydro-beta-carboline-3-carbo xylic acid [(-)-(1S,3S)-MNTCA], but the mutagen 4-(2-aminoethyl)-6-diazo-2,4-cyclohexadienone, produced from tyramine with nitrite, was one of the major products.

Carbolines↗
PubMed1983

Similarity between tyramine-induced neurotoxicity and the coma of Reye's syndrome.

The objective of the present investigation was to determine whether or not tyramine induces coma in experimental animals with impaired mitochondrial monoamine oxidase function, and whether the coma in these animals was a function of increased cerebrospinal fluid (CSF) pressure. Ten mongrel dogs were treated (orally) daily with the monoamine oxidase-inhibiting drug, phenelzine (4.5 mg/kg), over a period of 1 month. The present studies indicated that in phenelzine-treated animals with liver disease and behavioral side effects (n = 4), the i.v. administration of tyramine (1 mg/kg) caused substantial elevation in CSF pressure that exceeded 30 mm Hg (initial pressure 12.5 +/- 2.1). This was followed by substantial accumulation of tyramine, dopamine and norepinephrine concentrations in CSF of these animals. The animals became comatose soon afterward. The administration of tyramine to pretreated (n = 10) or phenelzine-treated animals without liver disease (n = 6) caused only the expected transient increase in blood pressure but with no significant effect on CSF pressure of these animals. These animals recovered fully from the experiment without any ill effect. These studies suggest that tyramine may have obvious implications in the development of intracranial hypertension in Reye's syndrome.

Animals↗
PubMed1978

Decarboxylation to tyramine: an important route of tyrosine metabolism in dogs with experimental hepatic encephalopathy.

Tyrosine metabolism via decarboxylation to tyramine was evaluated in dogs with functional end-to-side portacaval shunt. It was found that the endogenous plasma levels of both tyrosine and tyramine increased steadily after the construction of the shunt. These elevations became more pronounced when the dogs manifested symptoms of hepatic encephalopathy. In encephalopathic dogs, average endogenous plasma tyrosine and tyramine concentrations were 110.1 mumoles per liter and 7.6 ng per ml as compared to 55.4 and 1.2 in control dogs, respectively. The pattern of plasma concentrations of tyrosine and tyramine after an oral dose of L-tyrosine (50 mg per kg) was also investigated in control and shunted dogs. There was a progressive rise in peak levels of tyramine (to about 50-fold increase, at 6 weeks) after the construction of the shunt, as compared to levels obtained in pre- and at 1 and 4 weeks postoperatively (70.6 versus 1.20, 3.9, and 8.11 ng per ml). Similar observations were made with levels of plasma tyrosine. Six weeks after portacaval shunt, mean peak levels of plasma tyrosine, achieved at 5 hr after dose administration, were 450 as compared to 85 mumoles per liter obtained in preshunted dogs. These studies demonstrated a correlation between abnormalities in tyrosine metabolism and postshunt hepatic encephalopathy.

Amino Acids↗
PubMed1981

[Effects of parasympathetic drugs on head-twitch response induced by tyramine (author's transl)].

We investigated the effects of various parasympathetic drugs on the head-twitch response (HTR), as induced by intracerebroventricular (i.c.v.) administration of tyramine in mice pretreated with safrazine, a monoamine oxidase inhibitor. Intraperitoneal administration of neostigmine, methacholine, carbamylcholine, methylatropine or hexamethonium did not alter the HTR induced by tyramine. The i.c.v. infusion of acetylcholine, physostigmine, nicotine, carbamylcholine or atropine slightly inhibited the tyramine-response. The i.c.v. infusion of pilocarpine, methacholine, mechamylamine, hexamethonium or tetraethylammonium resulted in a slight or significant potentiation of the HTR. These results suggest that the HTR induced by tyramine is accelerated by mechanisms related to muscarinic receptors within the central nervous system and that the tyramine-response is suppressed by mechanisms related to nicotinic receptors.

Animals↗
PubMed1997

Inhibition of estrone sulfatase and proliferation of human breast cancer cells by nonsteroidal (p-O-sulfamoyl)-N-alkanoyl tyramines.

Estrogen levels in breast tumors of postmenopausal women are as much as 10 times higher than estrogen levels in plasma, presumably due to in situ formation of estrogen. The major source of estrogen in breast cancer cells may be the conversion of estrone sulfate to estrone by the enzyme estrone sulfatase. Thus, inhibitors of estrone sulfatase have potential for the treatment of estrogen-dependent breast cancers. Several steroidal agents have been developed that are potent estrone sulfatase inhibitors, most notably estrone-3-O-sulfamate. However, these compounds may be metabolized to forms that have undesired actions, including estrogenicity. To avoid the problems associated with a potentially active steroid nucleus, we designed and synthesized a series of (p-O-sulfamoyl)-N-alkanoyl tyramines as nonsteroidal estrone sulfatase inhibitors. These nine compounds differ in the length of their alkanoyl chains. We tested the ability of the (p-O-sulfamoyl)-N-alkanoyl tyramines to inhibit: (a) estrone sulfatase activity in intact cultures of human breast cancer cells (MDA-MB-231); and (b) the growth of estrogen-dependent human breast cancer cells (MCF-7). All of the test compounds (1 microM) inhibited the estrone sulfatase activity of intact MDA-MB-231 cells; however, compounds with a longer alkanoyl chain were more effective than those with a shorter chain. Dose-response analysis indicated an IC50 of 350 nM for (p-O-sulfamoyl)-N-tetradecanoyl tyramine for the inhibition of MDA-MB-231 estrone sulfatase activity. The inhibition of MDA-MB-231 cell estrone sulfatase activity by this compound was found to be irreversible. Cell proliferation assays involved the treatment of estrogen-deprived MCF-7 cells with test compounds (10 microM) in the presence of estrone sulfate (1 microM) as the only source of estrogen. All compounds inhibited cell proliferation to some extent, but the longer-chain analogues again were more effective. Dose-response analysis indicated an IC50 of 38 nM for (p-O-sulfamoyl)-N-tetradecanoyl tyramine for the inhibition of MCF-7 cell proliferation. Our data indicate the utility of (p-O-sulfamoyl)-N-alkanoyl tyramines for the inhibition of breast cancer cell estrone sulfatase activity. Furthermore, our data support the concept that nonsteroidal estrone sulfatase inhibitors may be useful as therapeutic agents for estrogen-dependent breast cancers.

Breast Neoplasms↗
PubMed1976

Release and receptor stimulating properties of p-tyramine in rat brain.

Radiolabeled p-tyramine could be released from rat striatal slices, which were previously allowed to accumulate this amine, upon depolarization with media containing 40 mM potassium. This depolarization-induced release did not occur in the absence of calcium ions in the medium and over 75% of the labeled material released was identified chromatographically as tyramine. The possible existence of a direct receptor-stimulating activity of p-tyramine was examined by injecting this amine intraventricularly into rats, after pretreatment with various drugs, which inhibit catecholaminergic function, and measuring their motor activity. If injected into rats, which were pretreated with reserpine or alpha-methyl-p-tyrosine, p-tyramine induced a marked increase in the motor activity, which was not accompanied by a significant decrease in brain catecholamines, ruling out the possibility of indirect receptor stimulation. Since the presence of endogenous p-tyramine in the brain has been reported, these data may indicate a specific synaptic role for this amine, perhaps as a neurotransmitter.

Animals↗
PubMed2000

Purification, cloning, and three-dimensional structure prediction of Micrococcus luteus FAD-containing tyramine oxidase.

The FAD-containing tyramine oxidase enzyme and gene from the Gram (+) bacterium Micrococcus luteus were isolated, and computer prediction was used to propose a preliminary 3D model of the protein. A 2.8-kb Sau3AI fragment containing the structural gene of tyramine oxidase was cloned from a M. luteus genomic DNA library. The 1332 bp gene encodes a protein of 443 amino acids, with a calculated molecular mass of 49.1 kDa. The enzyme was found to be a homodimer with a molecular weight of 49,000. It oxidizes tyramine, adrenaline, 3-hydroxytyramine, dopamine, and noradrenaline, and was reversibly inhibited by FAD-containing monoamine oxidase A and B specific inhibitors. Sequence comparison show that tyramine oxidase is smaller than other FAD-amine oxidases but that it contains well-conserved amino acid residues reported in all other FAD-amine oxidases. A hypothetical three-dimensional structure of tyramine oxidase has also been proposed based on secondary structure predictions, threading, and comparative modeling.

Amino Acid Sequence↗
PubMedDate not supplied

Acute and subacute toxicity of tyramine, spermidine, spermine, putrescine and cadaverine in rats.

The acute and subacute toxicity of five biogenic amines-tyramine, spermidine, spermine, putrescine and cadaverine-were examined in Wistar rats. Tyramine and cadaverine had a low acute oral toxicity of more than 2000 mg/kg body weight. Putrescine had an acute oral toxicity of 2000 mg/kg body weight and spermidine and spermine each of 600 mg/kg body weight. All amines investigated caused a dose-related decrease in blood pressure after intravenous administration, except for tyramine, where an increase was found. In 6-wk studies the biogenic amines were administered in the diet to groups of 10 male and 10 female rats. Tyramine and cadaverine were given at levels of 0, 200, 2000 or 10,000 ppm, spermine and putrescine at levels of 0, 200, 2000 or 5000 ppm and spermidine at levels of 0, 20, 200 or 500/1000 ppm in the first study and at levels of 0 or 10,000 ppm in a second study. Spermine was the most toxic. The high dose level showed a great number of changes, such as emaciation, aggressiveness, convulsions and paralysis of the hind legs. Growth, food intake and water intake were considerably decreased. Slight anaemia (males) and changes in plasma clinical chemistry occurred. The relative weights of the thyroid, adrenals, spleen and heart were increased and that of the liver decreased. Impaired kidney function, together with renal histopathological changes and changes in plasma electrolytes and urea, occurred with spermine. Histopathological examinations also revealed decreased glycogen content in the liver, reduction of spermatogenesis, severe depletion of splenic white pulp, acute involution of the thymus and moderate myocardial degeneration in the heart. Myocardial degeneration was also seen in one mid-dose male. Adverse effects were also observed in the top dose groups of all other amines. Decreased body weights associated with diminished food intake were generally seen. Slight increases in packed cell volume, haemoglobin concentration and thrombocytes occurred with cadaverine. With spermidine, decreased plasma creatinine, calcium and inorganic phosphate were observed and decreased potassium levels with cadaverine. The no-observed-adverse-effect level was 2000 ppm (180 mg/kg body weight/day) for tyramine, cadaverine and putrescine, 1000 ppm (83 mg/kg body weight/day) for spermidine and 200 ppm (19 mg/kg body weight/day) for spermine.

Administration, Oral↗
PubMed2005

Two functional but noncomplementing Drosophila tyrosine decarboxylase genes: distinct roles for neural tyramine and octopamine in female fertility.

The trace biogenic amine tyramine is present in the nervous systems of animals ranging in complexity from nematodes to mammals. Tyramine is synthesized from tyrosine by the enzyme tyrosine decarboxylase (TDC), a member of the aromatic amino acid family, but this enzyme has not been identified in Drosophila or in higher animals. To further clarify the roles of tyramine and its metabolite octopamine, we have cloned two TDC genes from Drosophila melanogaster, dTdc1 and dTdc2. Although both gene products have TDC activity in vivo, dTdc1 is expressed nonneurally, whereas dTdc2 is expressed neurally. Flies with a mutation in dTdc2 lack neural tyramine and octopamine and are female sterile due to egg retention. Although other Drosophila mutants that lack octopamine retain eggs completely within the ovaries, dTdc2 mutants release eggs into the oviducts but are unable to deposit them. This specific sterility phenotype can be partially rescued by driving the expression of dTdc2 in a dTdc2-specific pattern, whereas driving the expression of dTdc1 in the same pattern results in a complete rescue. The disparity in rescue efficiencies between the ectopically expressed Tdc genes may reflect the differential activities of these gene products. The egg retention phenotype of the dTdc2 mutant and the phenotypes associated with ectopic dTdc expression contribute to a model in which octopamine and tyramine have distinct and separable neural activities.

Amino Acid Sequence↗
PubMed1995

Partial Purification and Characterization of Hydroxycinnamoyl-Coenzyme A:Tyramine Hydroxycinnamoyltransferase from Cell Suspension Cultures of Solanum tuberosum.

A pathogen elicitor-inducible soluble acyltransferase (tyramine hydroxycinnamoyltransferase [THT], EC 2.3.1), which catalyzes the transfer of hydroxycinnamic acids from hydroxycinnamoyl-coenzyme A (CoA) esters to tyramine in the formation of N-hydroxycinnamoyltyramine, was partially purified with a 380-fold enrichment and a 6% recovery from cell-suspension cultures of potato (Solanum tuberosum L. cv Datura). The enzyme showed specific activities of 33 mkat (kg protein)-1 (formation of feruloyltyramine). The apparent native Mr was found to be approximately 49,000. Highest activity was at pH 6.8 in K-phosphate. The isoelectric point of the enzyme was approximately pH5.2. The apparent energy of activation was calculated to be 96 kJ mol-1. The enzyme activity was stimulated more than 5-fold by 10 mM Ca2+ or Mg2+. The apparent Km values were 36 [mu]M for feruloyl-CoA and 85 and 140 [mu]M for cinnamoyl- and 4-coumaroyl-CoA, respectively. The Km value for tyramine in the presence of feruloyl-CoA was 22 [mu]M. In the presence of 4-coumaroyl-CoA, however, the Km for tyramine increased to about 230 [mu]M. The mode of action was an iso-ordered bi bi mechanism in which A, B, P, and Q equal hydroxycinnamoyl-CoA, tyramine, N-hydroxycinnamoyltyramine, and CoA, respectively. Thus, the reaction occurred in a ternary complex of the enzyme and substrates. The equilibrium constant of the reaction was determined to be 1.3 x 104. This gave a [delta]G[deg][prime] eq value of -23.5 kJ mol-1.

Journal Article↗
PubMed1999

Signal amplification in flow cytometry using biotin tyramine.

BACKGROUND: Catalysed reporter deposition (CARD) has been successfully used as a means of signal amplification in solid-phase immunoassays. The procedure relies on the use of horseradish peroxidase (HRP)-conjugated reagents--normally antibodies-in conjunction with substituted phenolic compounds such as biotin tyramine. The HRP catalyses deposition of biotin tyramine around the site of enzyme activity, and streptavidin-HRP can then be added to generate an amplified HRP signal. The possibility of using this technique for solution-phase amplifications has been suggested but not yet demonstrated. METHODS: This paper describes the application of CARD to signal enhancement in flow cytometry. The specific examples described here are those of anti-human CD4 and anti-human CD36 antibodies binding to either human lymphocytes or mixed mononuclear cells. RESULTS: Optimum biotin tyramine concentrations were evaluated, and a fivefold increase in signal was observed over standard detection of the anti-human CD4 antibody with anti-mouse-fluorescein isothiocyanate (FITC). In the example using the anti-CD36 antibody, the biotin tyramine treatment was repeated, resulting in an additional 2.5-fold signal amplification. CONCLUSIONS: The technique described in this report provides a method of amplifying the signals achieved by standard flow cytometry detection reagents.

Biotin↗
PubMed1997

Pressor response to tyramine after single 24-hour application of a selegiline transdermal system in healthy males.

Orally administered selegiline hydrochloride is a selective monoamine oxidase type B inhibitor at the recommended regimen of 10 mg/day, but it loses selectivity at higher doses. In bypassing first-pass metabolism, a 24-hour application of transdermally administered selegiline (7.8 mg/24 hr) yields fifty times greater systemic exposure than is provided by single oral doses. The current study was designed to demonstrate that, similar to the oral regimen, transdermally administered selegiline is devoid of the pressor effects associated with tyramine and classic monoamine oxidase type A inhibitors. A single-blind, staggered, parallel-group study of pressor response to tyramine during a single 24-hour application of one-quarter, one-half, or one selegiline transdermal system relative to baseline (drug-free) response to tyramine was conducted in three groups, each with five healthy male volunteers. The end point of pressor response was declared if a participant's systolic blood pressure rose by > 30 mmHg, heart rate decreased by > 25 bpm with an associated > 20-mmHg rise in systolic blood pressure, or a clinically significant change was observed in the electrocardiogram. Doses up to 600 mg were administered during the baseline phase and up to 200 mg during the active-treatment phase. Participants received escalating tyramine doses every 4 hours until the maximum or threshold dose was achieved. Doses up to 200 mg were tolerated without apparent increase in sensitivity in participants receiving one-quarter, one-half, or one selegiline transdermal system. All participants completed the trial, and no significant adverse events were reported. Monoamine oxidase type B inhibition was complete (100%) by 12 hours after initial application in all treatment groups while plasma levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) after 24-hour application were unaffected relative to baseline. These results suggest that systemic selegiline levels may not predict the propensity for a hypertensive crisis associated with presumed nonselective doses and that the avoidance of peripheral monoamine oxidase type A inhibition in the gut via the selegiline transdermal system may provide a safe vehicle for administering selegiline at plasma levels beyond that which can be safely obtained after oral administration. These findings will need to be confirmed in a long-term dose setting.

Administration, Cutaneous↗