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PubMed2003

Determination of tyramine in cheese by LC-UV.

An isocratic reversed-phase liquid chromatographic assay for tyramine has been developed. The method is based on the reaction of tyramine with 4-chloro-7-nitrobenzofurazan and measurement of the absorbance at 458 nm after chromatographic separation on a C-18 column. Optimum reaction conditions were investigated. A linear relationship was found between absorbance and concentration over the range 25-300 ng per 10 microl of tyramine. The method was applied to the determination of tyramine in cheese. The cheese sample was homogenized with 5% (w/v) HClO(4) extracted with ethyl acetate-acetone (2:1) and chromatographed on high performance liquid chromatography (HPLC) after derivatization reaction with NBD-Cl. The determination limit was 25 microg/g cheese. The mean recovery of tyramine from cheese was 98.0%.

Cheese↗
PubMed2006

Early PCR detection of tyramine-producing bacteria during cheese production.

Biogenic amines (BA) are toxic substances that appear in foods and beverages. Tyramine is the most abundant BA in cheeses. A PCR method was developed to detect the presence of tyramine-producing bacteria during cheese manufacture and ripening. Six different batches of a farmhouse blue cheese were analysed by PCR. Tyramine concentrations were also determined by HPLC. The PCR method was able to anticipate tyramine accumulation in the cheeses; the presence of tyramine-producing microorganisms in the early stages of manufacture correlated well with a high concentration of BA in mature cheese samples.

Cheese↗
PubMed1992

Comparison of the pressor effect of tyramine after treatment with phenelzine and moclobemide in healthy male volunteers.

This study was conducted to establish the safety, tolerability, side effects, and pressor effects of tyramine on subjects treated with moclobemide, a short-acting reversible and preferential monoamine oxidase inhibitor, and to compare these responses with the responses of subjects treated with phenelzine. Twelve healthy male volunteers participated. An oral tyramine sensitivity test was performed on all subjects 24 hours before the start of a 28-day open-label treatment with phenelzine or moclobemide. A tyramine challenge was performed on day 28 on four subjects treated with phenelzine. The mean dose of oral tyramine required to increase systolic blood pressure by 30 mm Hg was 15 mg. The mean dose of tyramine that produced a clinical response (day 28) in subjects treated with moclobemide was 240 mg. No subject receiving moclobemide responded clinically on day 31 after receiving hourly doses of 20, 40, 80, 160, and 320 mg, respectively. These findings suggest that moclobemide may be used without stringent dietary precautions.

Administration, Oral↗
PubMed1977

The biosynthesis of tyramine glucuronide by liver microsomal fractions.

Labelled tyramine glucuronide was synthesized in vitro from UDP-[14C]glucuronic acid, [14C]tyramine or [3H]tyramine. The glucuronidation was carried out at pH9.2 in the presence of a monoamine oxidase inhibitor, trans-2-phenylcyclopropylamine. The Km values for tyramine were 69 and 125 micrometer and those for UDP-glucuronic acid were 260 and 290 micrometer respectively for guinea-pig and rat liver microsomal preparatons. The specific activities of microsomal glucuronyltransferase measured in fresh hepatic preparations of guinea pig, mouse and rat were respectively 601, 251 and 235 pmol of [14C]tyramine glucuronide/min per mg of protein. Increase in activity ranged from 2- to 6-fold in preparations which were frozen and thawed once and 5.4- to 10-fold when the freezing and thawing was repeated. Rabbit liver has very low activity, and monkey liver and intestine were completely devoid of this conjugating capacity.

Animals↗
PubMed2000

Amtyr1: characterization of a gene from honeybee (Apis mellifera) brain encoding a functional tyramine receptor.

Biogenic amine receptors are involved in the regulation and modulation of various physiological and behavioral processes in both vertebrates and invertebrates. We have cloned a member of this gene family from the CNS of the honeybee, Apis mellifera. The deduced amino acid sequence is homologous to tyramine receptors cloned from Locusta migratoria and Drosophila melanogaster as well as to an octopamine receptor cloned from Heliothis virescens. Functional properties of the honeybee receptor were studied in stably transfected human embryonic kidney 293 cells. Tyramine reduced forskolin-induced cyclic AMP production in a dose-dependent manner with an EC50 of approximately 130 nM. A similar effect of tyramine was observed in membrane homogenates of honeybee brains. Octopamine also reduced cyclic AMP production in the transfected cell line but was both less potent (EC50 of approximately 3 microM) and less efficacious than tyramine. Receptor-encoding mRNA has a wide-spread distribution in the brain and subesophageal ganglion of the honeybee, suggesting that this tyramine receptor is involved in sensory signal processing as well as in higher-order brain functions.

Amino Acid Sequence↗
PubMed1996

Tyramine content of previously restricted foods in monoamine oxidase inhibitor diets.

Traditional monoamine oxidase inhibitors (MAOIs) remain an important class of drugs for a variety of psychiatric conditions, including depressive illnesses, anxiety, and eating disorders. It was the objective of this study to refine the MAOI diet by determining the tyramine content of a variety of untested and "controversial" foods that continue to appear on MAOI diet-restricted food lists. A secondary objective of the study was to evaluate the effect of freshness on the tyramine content of some foods. Fifty-one food samples were evaluated for tyramine content by liquid chromatography. Food samples included a selection of sausages, beverages, sliced meat products, including chicken liver, and some fruits, including raspberries, bananas, and banana peels. Foods that were found to have dangerously high concentrations of tyramine (> or = 6 mg/serving) included chicken liver aged 9 days (63.84 mg/30 g), air-dried sausage (7.56 g/30 g), soy sauce (0.941 mg/ml), and sauerkraut (7.75 mg/250 g). Of the foods analyzed in this study, only those with high tyramine content per serving should continue to be absolutely restricted. All other foods are either safe for consumption or safe in moderation. The data provided should be combined with the data from other similar analytical studies to develop a list of foods that should be absolutely restricted. A more accurate list of restricted foods may enhance patient dietary compliance.

Diet Therapy↗
PubMed2003

Pressor response to intravenous tyramine is a marker of cardiac, but not vascular, adrenergic function.

Intravenous injections of the indirect sympathetic amine, tyramine, are used as a test of peripheral adrenergic function. The authors measured the time course of increases in ejection fraction, heart rate, systolic and diastolic pressure, popliteal artery flow, and greater saphenous vein diameter before and after an injection of 4.0 mg/m(2) body surface area of tyramine in normal human subjects. The tyramine caused moderate, significant increases in systolic pressure and significant decreases in total peripheral resistance. The earliest changes were a 30% increase in ejection fraction and a 16% increase in systolic pressure, followed by a 60% increase in popliteal artery flow and a later 11% increase in greater saphenous vein diameter. There were no changes in diastolic pressure or heart rate. These results suggest that pressor responses during tyramine injections are primarily due to an inotropic response that increases cardiac output and pressure and causes a reflex decrease in vascular resistance. Thus, tyramine pressor tests are a measure of cardiac, but not vascular, sympathetic function.

Adult↗
PubMed1991

COMT inhibition with nitecapone does not affect the tyramine pressor response.

Nitecapone (OR-462) is a new selective COMT inhibitor with gastroprotective properties. The aim of the present study was to determine whether nitecapone potentiates the haemodynamic effects of a tyramine-induced increase in catecholamine release. The systolic blood pressure response to tyramine was studied in 11 healthy male volunteers (age 20-32 years). Tyramine was given i.v. as rapid bolus injections in increasing doses without drug intake and after oral intake of single doses of 25 mg and 100 mg of nitecapone. The tyramine dose required to increase systolic blood pressure by 30 mm Hg ('pressor dose') was 4.98 mg, 5.04 mg and 4.88 mg after no medication, and with 25 mg and 100 mg of nitecapone, respectively. There were also no differences in the systolic blood pressure response vs time curves between the three regimens. COMT inhibition with nitecapone did not potentiate the haemodynamic responses to tyramine-induced catecholamine release.

Adult↗
PubMed1994

Production of histamine and tyramine by lactic acid bacteria isolated from vacuum-packed sugar-salted fish.

The incidence of histamine- or tyramine-producing lactic acid bacteria was examined in several products of vacuum-packed sugar-salted fish (salmon, halibut, mackerel). No histamine-producing isolates were observed, whereas the majority of tyramine-producing isolates were identified as Carnobacterium spp. These organisms were shown to be important members of the microbial flora during storage of vacuum-packed sugar-salted salmon at 5 degrees C. The amount of tyramine produced was reduced by lowering the temperature from 9 degrees C to 4 degrees C for all of five strains of carnobacteria or lactobacilli. The majority of tyramine was produced during the exponential growth phase for Carnobacterium piscicola N 5 and Lactobacillus viridescens N 69. The ability of these bacteria to produce tyramine may be used as an index of microbial quality/acceptability of stored vacuum-packed sugar-salted fish.

Fish Products↗
PubMed1990

Monoamine oxidase (MAO)-A but not MAO-B inhibitors potentiate tyramine-induced catecholamine release from PC12 cells.

The previous report that PC12 (pheochromocytoma) cells have a K(+)-induced, as well as a tyramine-induced, catecholamine release mechanism has been confirmed. Selective monoamine oxidase (MAO)-A (clorgyline and moclobemide) and not MAO-B inhibitors (l-deprenyl, AGN 1135, and Ro 16-6491) potentiate the catecholamine-releasing action of tyramine significantly more than that of K+. The potentiation of tyramine-induced [3H]noradrenaline release from PC12 cells by MAO-A inhibitors has been linked to the presence of MAO-A in these cells, for which tyramine and noradrenaline are substrates. In the above respects, it is the PC12 cell that resembles more closely the peripheral adrenergic neuron, rather than the chromaffin cell, which is endowed with MAO-B and lacks the tyramine-releasable pool of catecholamines.

Animals↗
PubMed1968

The effects of drugs inhibiting catecholamine uptake on tyramine and noradrenaline-induced contractions of the isolated rat vas deferens.

1. Cocaine did not antagonize the tyramine-induced contractile response of the isolated rat vas deferens at the same concentrations which markedly potentiated the contractile response to noradrenaline.2. Imipramine and amitriptyline non-competitively antagonized the contractile response to tyramine but did not potentiate noradrenaline. Desmethylimipramine produced both potentiation of noradrenaline and antagonism of tyramine.3. Dexchlorpheniramine non-competitively antagonized the contractile response to tyramine. It also produced an atypical potentiation of noradrenaline in which lower concentrations of noradrenaline were potentiated to a greater extent than higher ones.4. Imipramine inhibited the in vitro uptake of noradrenaline-(3)H in rat vas deferens as did cocaine, desmethylimipramine and dexchlorpheniramine. These results suggest that the alpha-adrenergic blocking property of imipramine masks the potentiation of noradrenaline by uptake inhibition.5. Evidence is also presented which suggests that alpha-adrenergic blockade of released noradrenaline may be the major mechanism for tyramine inhibition by imipramine-like drugs. This may explain why cocaine, which has no real alpha blocking action, is ineffective against tyramine.

Animals↗
PubMed1969

The effect of cocaine and imipramine on tyramine-induced release of noradrenaline-3H from the rat vas deferens in vitro.

1. Tyramine 10(-4)M significantly increased release of noradrenaline-7-(3)H (NA-7-(3)H) from rat vas deferens in vitro.2. Neither cocaine 10(-5)M nor imipramine 10(-7)M-10(-6)M significantly reduced tyramine-induced release of NA-7-(3)H.3. Increasing the exposure time to cocaine and imipramine from 10 to 20 min or pre-incubating the tissue with a wide range of NA-7-(3)H concentrations (3.3-333.3 ng/ml.) did not affect the lack of inhibition by cocaine and imipramine.4. It is suggested that the tyramine receptor in rat vas deferens differs from that in other systems and that blockade of tyramine-released noradrenaline at alpha-adrenergic receptors may be the most important mechanism for tyramine antagonism by imipramine-like drugs in this tissue.

Animals↗
PubMed2002

Tyramine stimulates glucose uptake in insulin-sensitive tissues in vitro and in vivo via its oxidation by amine oxidases.

Tyramine and benzylamine have been described as stimulators of glucose transport in adipocytes. This effect is dependent on amine oxidation by monoamine oxidase (MAO) or semicarbazide-sensitive amine oxidase (SSAO) and on the subsequent hydrogen peroxide formation as already demonstrated by blockade with oxidase inhibitors or antioxidants and potentiation with vanadate. In this work, we extended these observations to skeletal muscle and cardiac myocytes using in vitro and in vivo approaches. Tissue distribution studies showed that substantial extrahepatic peripheral MAO activities exist in kidney and gut, but also in insulin-sensitive tissues: heart, adipose tissue, and skeletal muscles. SSAO activity is also widely distributed and present at a lower level than MAO, except in fat depots where both oxidases were equally involved in tyramine oxidation. When tested in vitro at millimolar doses, tyramine caused a large stimulation of glucose transport in rat adipocytes and in skeletal and cardiac muscles. In vivo administration of tyramine (4 mg/kg i.p.) lowered the hyperglycemic responses to a glucose challenge in control and in streptozotocin-treated rats. This positive effect on glucose disposal was obtained without vanadate and was abolished by SSAO and MAO inhibitors. Tyramine increased hexose uptake in vivo in insulin-sensitive tissues, whereas it induced only transient effects on plasma insulin or cardiovascular parameters. In conclusion, activation of the amine oxidases present in insulin-sensitive tissues induces insulin-like effects, readily detectable in vitro, and increasing peripheral glucose utilization in vivo.

Amine Oxidase (Copper-Containing)↗
PubMed1979

Arylsulfatase in Salmonella typhimurium: detection and influence of carbon source and tyramine on its synthesis.

Arylsulfatase synthesis was shown to occur in Salmonella typhimurium LT2. The enzyme had a molecular weight of approximately 50,000 and was separated into five forms by isoelectrofocusing. The optimal pH for substrate hydrolysis was pH 6.7, with Michaelis constants for nitrocatechol sulfate and nitrophenyl sulfate being 4.1 and 7.9 mM, respectively. Enzyme synthesis was strongly influenced by the presence of tyramine in the growth medium. The uptake of [14C]tyramine and arylsulfatase synthesis were initiated during the second phase of a diauxie growth response, when the organism was cultured with different carbon sources. Adenosine 3',5'-cyclic monophosphoric acid enhanced the uptake of tyramine and the levels of arylsulfatase synthesized. However, the addition of glucose and glycerol to organisms actively transporting tyramine and synthesizing enzyme caused a rapid inhibition of both of these processes. This inhibition was not reversed by adding adenosine 3',5'-cyclic monophosphoric acid. The results suggest that the effect of the carbon source on tyramine transport and arylsulfatase synthesis may be explained in terms of inducer exclusion.

Ammonium Chloride↗
PubMed1984

Metabolic responses to tyramine and cold in young male Sprague-Dawley and Fischer 344 rats.

Significant differences in responses to intraperitoneally injected tyramine or cold exposure (-10 degrees C) were observed in young (3-4 mo) male Sprague-Dawley (S-D) and Fischer 344 (F344) rats cold-acclimated (CA) or non-cold-acclimated (non-CA). Non-CA S-D and F344 rats respond to tyramine by increased O2 uptake and elevation of colonic temperature, but, as we had reported previously, the optimal doses of tyramine required was significantly different for these two strains, i.e., 2 mg/kg for F344 vs. 20 mg/kg for S-D. The response to tyramine was significantly potentiated by cold acclimation in both strains of rats. Despite the different dosages of tyramine given to the animals, similar increases in O2 uptakes and colonic temperatures were observed. Differences between these two strains were also evident in their responses to a cold challenge (3 h, -10 degrees C). The ranking for cold tolerance (-10 degrees C) was as follows: CA F344 greater than non-CA F344 greater than CA S-D greater than non-CA S-D. These differences between the two strains suggest that interpretations regarding the response of rats to stressful conditions must be made with caution and appreciation of strain differences.

Acclimatization↗
PubMed1981

Compartmental analysis of tyramine-induced norepinephrine depletion.

Tyramine-dependent depletion of norepinephrine was shown to occur from a single kinetically defined compartment. The kinetics of depletion were related to the tyramine concentration and were independent of the amount of norepinephrine within the neuron. Tyramine depleted equivalent amounts of norepinephrine from cytoplasmic, biosynthetic, stable and labile intraneuronal storage compartments by a cocaine-sensitive process. The norepinephrine specific activity of the thoracic aorta remained constant even after greater than 80% depletion due to tyramine. The results show no evidence for a tyramine-resistant pool(s) of norepinephrine within adrenergic neurons.

Animals↗
PubMedDate not supplied

Inhibition of lentil copper/TPQ amine oxidase by the mechanism-based inhibitor derived from tyramine.

Copper amine oxidase from lentil (Lens esculenta) seedlings was shown to catalyze the oxidative deamination of tyramine and three similar aromatic monoamines, benzylamine, phenylethylamine and 4-methoxyphenylethylamine. Tyramine, an important plant intermediate, was found to be both a substrate and an irreversible inhibitor of the enzyme whereas the other amines were not inhibitory. In the course of tyramine oxidation the enzyme gradually became inactivated with the concomitant appearance of a new absorption at 560 nm due to the formation of a stable adduct. Inactivation took place only in the presence of oxygen and was probably due to the reaction of the enzyme with the oxidation product of tyramine, p-hydroxyphenylacetaldehyde. The kinetic data obtained in this study indicate that tyramine represents a new interesting type of physiological mechanism-based inhibitor for plant copper amine oxidases.

Amine Oxidase (Copper-Containing)↗
PubMed2003

Effects of moderate hypothermia on norepinephrine release evoked by ouabain, tyramine and cyanide.

Using the dialysis technique, we examined the effect of moderate hypothermia on the norepinephrine efflux evoked by ouabain, tyramine and cyanide in anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and we measured the dialysate norepinephrine levels as an indicator of norepinephrine output at the cardiac sympathetic nerve endings. Through the dialysis probe, locally applied ouabain, tyramine and cyanide induced the norepinephrine efflux. The addition of desipramine (neuronal norepinephrine transport blocker, 100 microM) suppressed the norepinephrine efflux evoked by ouabain, tyramine and cyanide. This finding suggests that pharmacological agent-induced norepinephrine efflux was due to carrier-mediated outward norepinephrine transport. Moderate hypothermia (27.4 +/- 0.2 degrees C) caused suppression of the norepinephrine efflux evoked by ouabain, tyramine and cyanide. We conclude that moderate hypothermia suppresses the non-exocytotic norepinephrine release evoked by ouabain, tyramine and cyanide.

Animals↗