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PubMed1983

[Biogenic amines in food: effects of histamine, tyramine and phenylethylamine in the human].

The effect of 25 mg histamine, 25 mg tyramine and 5 mg phenylethylamine resp. in apple juice on 27 healthy volunteers was studied using a randomized placebo-controlled double-blind procedure. No statistically significant effect was found with histamine and tyramine, but phenylethylamine produced symptoms like headache, dizziness and discomfort in some volunteers. In a second experiment the effect of four different wines (2 dl) containing naturally several biogenic amines in various amounts (histamine n.d. - 21 ppm; tyramine 1-23 ppm; phenylethylamine n.d. - 6 ppm; putrescine 2-55 ppm) on 20 volunteers was recorded. The percentage of volunteers experiencing symptoms was of the same order of magnitude as in the first experiment. No correlation was found to exist in this second experiment between the occurrence of symptoms and the concentration of biogenic amines in the wine samples.

Beverages↗

PubMed1997

Isolation and characterization of highly (R)-specific N-acetyl-1-phenylethylamine amidohydrolase, a new enzyme from Arthrobacter aurescens AcR5b.

A new amidohydrolase deacetylating several N-acetyl-1-phenylethylamine derivatives (R)-specifically was found in Arthrobacter aurescens AcR5b. The strain was isolated from a wet haystack by enrichment culture with (R)-N-acetyl-1-phenylethylamine as the sole carbon source. (R) and (S)-N-acetyl-1-phenylethylamine do not serve as inducers for acylase formation. By improving the growth conditions the enzyme production was increased 47-fold. The amidohydrolase was purified to homogeneity leading to a 5.2-fold increase of the specific activity with a recovery of 67%. A molecular mass of 220 kDa was estimated by gel filtration. Sodium dodecyl sulfate/polyacrylamide gel electrophorosis shows two subunits with molecular masses of 16 kDa and 89 kDa. The optimum pH and temperature were pH 8 and 50 degrees C, respectively. The enzyme was stable in the range of pH 7-9 and at temperatures up to 30 degrees C. The enzyme activity was inhibited by Cu2+, Co2+, Ni2+, and Zn2+, and this inhibition was reversed by EDTA.M.

Amidohydrolases↗

PubMed1990

High-performance liquid chromatographic determination of beta-phenylethylamine in human plasma with fluorescence detection.

A simple and highly sensitive method for the determination of beta-phenylethylamine in human plasma is investigated. The method employs high-performance liquid chromatography with fluorescence detection. beta-Phenylethylamine and p-methylbenzylamine (internal standard) in human plasma are isolated by cation-exchange chromatography on a Toyopak SP cartridge and then converted into the corresponding fluorescent derivatives with 3,4-dihydro-6,7-dimethoxy-4-methyl-3-oxoquinoxaline-2-carbonyl chloride, a fluorescence derivatization reagent for amines. The derivatives are separated within 30 min on a reversed-phase column, TSK gel ODS-120T, with isocratic elution, and detected fluorometrically. The detection limit of beta-phenylethylamine is 0.3 pmol/ml in plasma (S/N = 3).

Benzylamines↗

PubMed1991

Beta-adrenoceptors and antidepressants: possible 2-phenylethylamine mediation of chronic phenelzine effects.

Effects of chronic administration of antidepressant drugs on beta-adrenoceptor function were assessed. Tricyclics (imipramine 30 mg/kg/day, desipramine 5 and 10 mg/kg/day) and monoamine oxidase inhibitors [(+/-)-tranylcypromine 1 mg/kg/day, phenelzine 5 and 10 mg/kg/day] were administered to Male Sprague-Dawley rats (n = 8), via Alzet 2ML2 osmotic minipumps for 28 days. Pumps were implanted subcutaneously in the interscapular region and replaced after 14 days. On days 21 and 22 motor-suppressant actions of the beta-adrenoceptor agonist salbutamol (3 mg/kg intraperitoneally [IP]) were assessed as a measure of beta-adrenergic receptor sensitivity. On day 28 the animals were killed and their brains used for measurement of drug levels and monoamine oxidase activity. Liver tissue was used to measure the trace amine 2-phenylethylamine. Each drug induced a decrease in the response to salbutamol. With phenelzine the decreased response to salbutamol was not observed at the lower dose. Differences in monoamine oxidase inhibition following phenelzine did not correspond to differential effects on functional beta-adrenergic sensitivity. Levels of 2-phenylethylamine, an endogenous amine that is also a metabolite of phenelzine, were significantly higher in the 10-mg/kg/day phenelzine group. These data suggest that 2-phenylethylamine may be one mediator of the chronic actions of phenelzine on beta-adrenoceptors.

Albuterol↗

PubMed1991

Amphetamine-antagonistic properties of 4-phenyl-1,2,3,4- tetrahydroisoquinoline: inhibition of spinal reflex-enhancing effects of methamphetamine, phenylethylamine and nomifensine.

The antagonistic effects of 4-phenyl-1,2,3,4-tetrahydroisoquinoline (4PTIQ) against S(+)-methamphetamine, phenylethylamine and nomifensine were studied by measurement of spinal monosynaptic reflex potential (MSR). S(+)-Methamphetamine, phenylethylamine and nomifensine enhanced the amplitude of MSR in C1-spinalized rats through release of noradrenaline from the terminals of descending fibers and consequent activation of alpha 1-adrenoceptors. Although 4PTIQ alone did not change the amplitude of the MSR, 4PTIQ inhibited the enhancement of MSR induced by S(+)-methamphetamine and related compounds. The MSR of rats with an intact spinal cord was enhanced by conditioning stimulation of the ipsilateral locus ceruleus. The MSR enhancement produced by the stimulation was blocked by prazosin but unaffected by 4PTIQ, showing that 4PTIQ does not have an alpha 1-blocking action. These results suggest that the antagonistic effects of 4PTIQ on MSR enhancement by S(+)-methamphetamine, phenylethylamine and nomifensine are due to its blocking of noradrenaline release produced by these amphetamine-like agents.

Amphetamine↗

PubMed1983

Differential effects of d-amphetamine, beta-phenylethylamine, cocaine and methylphenidate on the rate of dopamine synthesis in terminals of nigrostriatal and mesolimbic neurons and on the efflux of dopamine metabolites into cerebroventricular perfusates of rats.

The in vivo effects of four psychomotor stimulants (d-amphetamine, beta-phenylethylamine, cocaine and methylphenidate) were determined on: 1) the rate of dopamine (DA) synthesis, as measured by the accumulation of dihydroxyphenylalanine (DOPA) after aromatic L-amino acid decarboxylase inhibition, in the striatum (terminals of nigrostriatal neurons) and in the nucleus accumbens and olfactory tubercle (terminals of mesolimbic neurons) and 2) the efflux of the DA metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) into cerebroventricular perfusates of conscious, freely-moving rats. d-Amphetamine and beta-phenylethylamine produced biphasic responses with lower doses of each drug increasing both the efflux of DOPAC and the rate of DA synthesis in the striatum. Higher doses of each drug either had no effect or actually decreased the efflux of DOPAC and also decreased the rate of DA synthesis in the striatum. On the other hand, cocaine and methylphenidate only decreased the efflux of DOPAC and the rate of DA synthesis in the striatum. The effects of the drugs on the rate of DA synthesis in the nucleus accumbens and olfactory tubercle were similar to, but less pronounced than those seen in the striatum. These results are consistent with the following suggestions: 1) low doses of d-amphetamine and beta-phenylethylamine facilitate the neuronal release of DA while higher doses of both drugs facilitate release and inhibit neuronal reuptake of the amine, and 2) cocaine and methylphenidate preferentially block the neuronal reuptake of DA.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1986

beta-phenylethylamine effect on brain and blood catechol-O-methyltransferase activity.

A significant decrease in catechol-o-methyltransferase (COMT) activity has been found in the striatum (77% of control) and hippocampus (63% of control) of gerbils treated with daily injections of beta-phenylethylamine (50 mg/kg) for 10 days. This treatment group also exhibited increased (204% above control) COMT activity in a lysed red blood cell preparation. There were no changes in COMT activity in groups receiving 10 mg/kg beta-phenylethylamine or haloperidol (0.5 mg/kg). In vitro beta-phenylethylamine has no demonstrable effect on COMT activity.

Animals↗

PubMed1996

Urinary phenylethylamine and cortisol levels in the early puerperium.

Phenylethylamine and cortisol were measured in 24-h urine samples taken from women day 2/3 postpartum, and matched controls. They also completed self-rating blues and highs scales. There was no significant difference in phenylethylamine excretion in those who scored highly with blues or highs, and either postpartum or normal controls. The number of raised values for phenylethylamine output was significantly greater in the postpartum women, who had no psychopathology, than in normal controls. Cortisol levels were significantly raised in postpartum controls compared with normal controls; women with the highs excreted significantly less cortisol than other postpartum women.

Adolescent↗

PubMed1984

Analysis and the effects of some drugs on the metabolism of phenylethylamine and phenylacetic acid.

Phenylethylamine has been reliably measured using radioenzymatic, gas chromatographic, mass spectromatic and gas chromatographic - mass spectrometric methods. Phenylacetic acid has been measured using gas chromatographic and gas chromatographic-mass spectrometric methods. Phenylethylamine concentrations are increased primarily by phenylalanine, its amino acid precursor and by such monoamine oxidase inhibitors as L-deprenyl and pargyline. Phenylethylamine administration influences other neurotransmitters such as dopamine, norepinephrine and 5-hydroxytryptamine. It also effects the tyramines and possibly tryptamine.

Animals↗

PubMed1987

Rapid analysis of beta-phenylethylamine in tissues and body fluids utilizing pentafluorobenzoylation followed by electron-capture gas chromatography.

A rapid, sensitive gas chromatographic procedure for analysis of beta-phenylethylamine is reported. The procedure involves extraction with a liquid ion-pairing compound, back-extraction with HCl, basification and reaction with pentafluorobenzoyl chloride under aqueous conditions. The pentafluorobenzoyl derivative of beta-phenylethylamine is then separated and analyzed on a gas chromatograph equipped with a capillary column and an electron-capture detector. The procedure produces a derivative which has good chromatographic properties and a high degree of stability. The method has been applied to analysis of beta-phenylethylamine in a variety of tissues and body fluids.

Animals↗

PubMed1989

Hydroxylation of phenylethylamine by rat liver preparations. Inhibition studies.

1. Rat liver 100,000 g pellet microsomal fraction p-hydroxylate phenylethylamine to tyramine in a relatively slow proceeding, NADPH-requiring reaction; Km 2.1 x 10(-5) M and Vmax 0.32 nmol/mg protein/20 min. 2. This reaction is inhibited, either competitively, noncompetitively or uncompetitively by a number of behaviorally active monomethylated and monohalogenated derivatives of phenylethylamine. 3. Whereas formation of tyramine was not significantly affected by L-phenylalanine or its p-chloro derivative, it was competitively inhibited by imipramine, iprindole and alprazolam. 4. It is suggested that at least some of the effects of these drugs may result from their ability to interfere with phenylethylamine metabolism.

Animals↗

PubMed1995

High-performance liquid chromatographic analysis of beta-phenylethylamine for the estimation of in vivo protein synthesis.

A rapid, sensitive, and automated reversed-phase liquid chromatographic method was developed for the analysis of phenylalanine as beta-phenylethylamine, for the measurement of in vivo protein synthesis. beta-Phenylethylamine was derivatized with o-phthaldialdehyde (OPA) to form a fluorescent derivative that was successfully measured in tissue cell fluids and hydrolysates as the decarboxylation product of phenylalanine. The system was extremely sensitive enabling the accurate determination of 0.5 pmol in biological samples. Analysis time was less than 11 min, so that 130 samples can be analysed per day. The method eliminates the need for time-consuming column extraction procedures. This method offers substantial advantages over existing methods for the isolation and determination of beta-phenylethylamine.

Animals↗

PubMed1996

1-phenylethylamines: a new series of illicit drugs?

Since 1993 many seizures of 1-phenylethylamine have been made in several European countries. It was originally thought that 1-phenylethylamine had been made in error, but later information suggested that it had been prepared deliberately. The related compounds, 1-amino-1-(4-methylphenyl)ethane and 1-methylamino-1-phenylethane and the 1-propanamine isomer of 3,4-methylenedioxyamphetamine, have also occurred in isolated cases. Analytical data are presented on these amines as well as a number of Leuckart impurities in 1-phenylethylamine. The pharmacological effects of these substances are largely unknown.

Designer Drugs↗

PubMed2004

Is monoamine oxydase-B a modifying gene and phenylethylamine a harmful compound in phenylketonuria?

We report here very high urinary phenylethylamine level in a phenylketonuric newborn and variable phenylethylamine levels in phenylketonuric patients with similar phenylalanine levels. As phenylethylamine, a very toxic metabolite of phenylalanine, is rapidly degraded by monoamine oxydase type B, an enzyme that has a very low activity in neonates, these results are consistent with those of the hypothesis of MAO-B acting as a modifying gene in phenylketonuria.

Adult↗

PubMed1977

Urinary mandelic acid: identified in normal individuals following a single oral load of phenylethylamine.

1. An increased urinary mandelic acid was identified by gas-liquid chromatography in the urine of 3 healthy subjects following the oral ingestion of phenylethylamine. 2. The pathway for the formation of mandelic acid from phenylethylamine was suggested to involve the intermediate phenylethanolamine. The basic similarity of the metabolism of phenylethylamine and tyramine was suggested by the excretion of 4.5% of phenulethlamine as mandelic acid which correlated well to a reported 7.2% of p-tyramine excreted as p-hydroxy mandelic acid.

Humans↗

PubMed1978

Phenylethylamine overproduction in aggressive psychopaths.

Plasma concentrations of free and conjugated phenylacetic acid, the major metabolite of phenylethylamine, were higher in ten prisoners serving long terms of imprisonment for violent crimes than in pair-matched non-violent control prisoners. Since amphetamine, a compound closely related to phenylethylamine, can reduce aggressiveness in some violent subjects, the increase in phenylethylamine production may be an attempt to compensate for the unknown derangement of function responsible for increased aggression.

Adult↗

PubMed1981

The formation of azoxy-2-phenylethane during the biological oxidation of phenylethylamine by rabbit liver microsomes.

Incubation of phenylethylamine with rabbit liver microsomes, divalent manganese and a NADPH generating system leads to the formation of azoxy-2-phenylethane, among other metabolic products. Approximately 38 nmol of the azoxy compound is formed form 10 mumol of phenylethylamine during a 30 min incubation. Azoxy-2-phenylethane was identified by comparison of its chromatographic (thin-layer, high pressure liquid and gas chromatography) properties with those of an authentic standard and was confirmed by mass spectrometry. The metabolism of phenylethylamine to azoxy-2-phenylethane appears completely dependent on the presence of divalent manganese; no reaction was observed in the absence of this metal or in the presence of equivalent concentrations of cupric ions. Azoxy-2-phenylethane was mutagenic, with S-9 activation, in S. typhimurium strains TA 100 and TA 1535 but not in TA 98 or TA 1537. This report constitutes the first demonstration of the formation of an aliphatic azoxy compound from the corresponding amine by a mammalian system.

Animals↗

PubMedDate not supplied

Preferential blockade of alpha 1-adrenoceptors in the rabbit pulmonary artery by derivatives of beta-phenylethylamine chemically related to BE 2254 (heat).

We investigated the antagonistic properties of several derivatives of beta-phenylethylamine at pre- and postsynaptic alpha-adrenoceptors (alpha 2 and alpha 1, respectively) using strips of rabbit pulmonary arteries preincubated with [3H]noradrenaline. The parent compound, BE 1726 [2-(beta-phenylethyl-aminomethyl)-tetralone], produced an increase in electrically evoked 3H overflow and in inhibition of the electrically evoked increase in tension; both effects occurred in the same concentration range. Substitution on the benzene ring of the beta-phenylethylamine moiety with a hydroxy (e.g., BE 2254, a well-characterized alpha 1-adrenoceptor antagonist) and/or methoxy group did not substantially alter the presynaptic potency, but considerably increased the potency at postsynaptic sites (some of the derivatives were as potent as prazosin). beta-Hydroxy substitution on the aliphatic chain selectively decreased the presynaptic potency. Hence, these changes in structure resulted in a marked preference for action at postsynaptic sites which was, however, less pronounced than that of prazosin. The increasing effect of the drugs on 3H overflow was attenuated by clonidine, and the compounds produced parallel shifts to the right of the concentration-response curve of noradrenaline for its contractile action, suggesting that the pre- and postsynaptic effects were mediated via alpha-adrenoceptors. In conclusion, strong and preferential blockade of alpha 1-adrenoceptors can be achieved by derivatives of beta-phenylethylamine, N-substituted with methyl-alpha-tetralone.

Adrenergic alpha-Antagonists↗