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PubMed1997

2-phenylethylamine catabolism by Escherichia coli K-12: gene organization and expression.

A gene encoding phenylacetaldehyde dehydrogenase (PAD), the enzyme involved together with a copper-topaquinone-containing amine oxidase in the initial steps of 2-phenylethylamine catabolism, was located at 31.1 min on the Escherichia coli K-12 genetic map. It was immediately adjacent to the gene encoding the amine oxidase but transcribed in the opposite direction. The purified PAD acted almost equally well on phenylacetaldehyde, 4-hydroxyphenylacetaldehyde and 3,4-dihydroxyphenylacetaldehyde. It had a subunit size of 54 kDa and its deduced amino acid sequence was approximately 40% identical to various eukaryotic and prokaryotic aldehyde dehydrogenases. A third gene encoding a positive regulatory protein required for expression of the amine oxidase and PAD genes was located next to the PAD gene. A gene previously located in this position was reported to encode a second amine oxidase but this was not confirmed. The nucleotide sequence from 1447 to 1450 kb on the E. coli K-12 physical map has been determined.

Aldehyde Oxidoreductases↗
PubMed2002

Diastereomeric salts of lactic acid and 1-phenylethylamine, their structures and relative stabilities.

Crystal structures have been determined for the two diastereomeric salts formed between S-lactic acid (S-LA) and 1-phenylethylamine (PEA). The relative stabilities of the salts have been investigated by differential scanning calorimetry and solubility measurements in acetonitrile. The less soluble salt obtained from water, (R-PEA)(S-LA), is the less dense. It belongs to the orthorhombic space group P2(1)2(1)2(1), Z = 4. The more soluble salt, (S-PEA)(S-LA) x H(2)O, crystallized from ethanol is monoclinic, space group P2(1), Z = 2. The crystal structure showed that the water molecule is well integrated into the hydrogen-bond network in the more soluble salt, which explains the fruitless attempts made to obtain the corresponding unhydrated salt. The lactate ion adopts different conformations in the two salts. The relative energies were investigated by Hartree-Fock calculations, showing that the lactate ion is in a conformation with higher energy in the more soluble salt. The difference in solubility between the two salts can be attributed to an interplay of enthalpy and entropy effects.

Journal Article↗
PubMed1981

Oxidation of beta-phenylethylamine by both types of monoamine oxidase: examination of enzymes in brain and liver mitochondria of eight species.

beta-Phenylethylamine (PEA) was characterized as a substrate for type A and type B monoamine oxidase (MAO) in brain and liver mitochondria of eight species at different substrate concentrations. In all species, at 10.0 microM, PEA was almost specific for type B MAO. At 1000 microM, however, the amine was common for both types of MAO in rat brain and liver, human brain and liver, mouse brain, guinea pig brain and liver, and bovine brain, while it was specific for type B MAO in mouse liver, rabbit brain and liver, bovine liver, pig brain and liver, and chicken brain and liver. From the present study, when PEA is used as a type B substrate, it is recommended that the substrate concentration should be sufficiently low to avoid the effects of species and tissue differences.

Animals↗
PubMed1986

Effects of deuterium substitution on the catabolism of beta-phenylethylamine: an in vivo study.

beta-Phenylethylamine (PE) hydrochloride injected intraperitoneally into rats was distributed evenly throughout the various regions of rat brain. Similarly, when a mixture of PE and alpha, alpha, beta, beta-deuterated PE [( 2H4]PE) was injected, no regional differences were observed in the ratios of the amounts of [2H4]PE and PE present; however, significantly more [2H4]PE than PE was present, although a 1:1 mixture had been administered. Further experiments in which the amounts of [2H4]PE and PE in whole rat brain, liver, and plasma were quantified confirmed this finding. The maximum [2H4]PE-to-PE ratios observed were 67 in whole brain 1 h after injection and 8 in liver and in plasma 45 min after injection. The whole brain [2H4]PE-to-PE ratios were decreased by pargyline pretreatment. Subsequent experiments showed that more alpha, alpha-[2H2]PE than PE was present in whole brain, liver, and plasma of rats injected with an equimolar mixture of alpha, alpha-[2H2]PE and PE. In contrast, beta, beta-[2H2]PE was not enriched in comparison to PE under the same experimental conditions. We concluded that the basis for the enrichment of [2H4]PE and alpha, alpha-[2H2]PE compared to PE was due to protection of the deuterated analogs from the actions of monoamine oxidase and perhaps aldehyde dehydrogenase; this protection led to pronounced deuterium substitution effects in vivo especially in the brain.

Animals↗
PubMed1987

Characterization of [3H]mazindol binding in rat brain: sodium-sensitive binding correlates with the anorectic potencies of phenylethylamines.

Saturable low-affinity binding sites for [3H]mazindol have been demonstrated in crude synaptosomal membranes from rat brain using both a centrifugation and a filtion assay. Studies on the regional distribution of these binding sites revealed that the hypothalamus and brainstem had the highest density of sites. Kinetic analysis of the binding of [3H]mazindol to hypothalamic membranes demonstrated a single class of noninteracting binding sites with an apparent affinity constant (KD) of 10.2 +/- 0.7 microM and maximal number of binding sites (Bmax) of 786 +/- 94 pmol/mg of protein. Specific [3H]mazindol binding was rapidly reversible, temperature sensitive, labile to pretreatment with proteolytic enzymes, and inhibited by physiological concentrations of sodium. In most peripheral tissues, such as the liver and kidney, very low levels of binding were observed; however, the adrenal gland had a relatively high density of sites. The potency of a series of anorectic drugs in inhibiting specific [3H]mazindol binding to hypothalamic membranes was highly correlated with their anorectic potencies in rats, but not with their motor stimulatory effects. These results suggest the presence of a specific drug recognition site in the hypothalamus that may mediate the anorectic activity of mazindol and related phenylethylamines.

Animals↗
PubMed2004

Dopamine transporter-dependent and -independent actions of trace amine beta-phenylethylamine.

Beta-phenylethylamine (beta-PEA) is an endogenous amine that is found in trace amounts in the brain. It is believed that the locomotor-stimulating action of beta-PEA, much like amphetamine, depends on its ability to increase extracellular dopamine (DA) concentrations owing to reversal of the direction of dopamine transporter (DAT)-mediated DA transport. beta-PEA can also bind directly to the recently identified G protein-coupled receptors, but the physiological significance of this interaction is unclear. To assess the mechanism by which beta-PEA mediates its effects, we compared the neurochemical and behavioral effects of this amine in wild type (WT), heterozygous and 'null' DAT mutant mice. In microdialysis studies, beta-PEA, administered either systemically or locally via intrastriatal infusion, produced a pronounced outflow of striatal DA in WT mice whereas no increase was detected in mice lacking the DAT (DAT-KO mice). Similarly, in fast-scan voltammetry studies beta-PEA did not alter DA release and clearance rate in striatal slices from DAT-KO mice. In behavioral studies beta-PEA produced a robust but transient increase in locomotor activity in WT and heterozygous mice. In DAT-KO mice, whose locomotor activity and stereotypy are increased in a novel environment, beta-PEA (10-100 mg/kg) exerted a potent inhibitory action. At high doses, beta-PEA induced stereotypies in WT and heterozygous mice; some manifestations of stereotypy were also observed in the DAT-KO mice. These data demonstrate that the DAT is required for the striatal DA-releasing and hyperlocomotor actions of beta-PEA. The inhibitory action on hyperactivity and certain stereotypies induced by beta-PEA in DAT-KO mice indicate that targets other than the DAT are responsible for these effects.

Animals↗
PubMed1976

Metabolism of phenylethylamine in rat isolated perfused lung: evidence for monoamine oxidase 'type B' in lung.

Phenylethylamine is inactivated in a single passage through rat lung tissue by a process of uptake and deamination by a monoamine oxidase 'type B'. This enzyme is particularly susceptible to inhibition by deprenil and less sensitive to clorgyline. The monoamine oxidase of the lung, like that of other rat tissues, can be differentiated into 'type A' and 'type B' which appear to operate independently in the organized tissue.

Animals↗
PubMed1976

Effects of mazindol, a non-phenylethylamine anorexigenic agent, on biogenic amine levels and turnover rate.

1 Mazindol is a new anorexigenic agent which possesses a different chemical structure from that of phenylethylamines, but shows a pharmacological profile similar to that of (+)-amphetamine. 2 Mazindol neither altered whole brain monoamine levels (noradrenaline (NA), dopamine, 5-hydroxytryptamine (5-HT)) nor changed NA levels in the hypothalamus or dopamine levels in the caudate nucleus. 3 Mazindol enhanced dopamine turnover rate in the caudate nucleus, as shown by the increased rate of dopamine decline after blockade of catecholamine synthesis by alpha-methyl-p-tyrosine and decreased the conversion index of (3H)-tyrosine into brain NA. 4 Mazindol administration did not modify pargyline-induced decline of 5-hydroxyindoleacetic acid suggesting that 5-HT turnover is not altered by this drug.

Animals↗
PubMed1979

The metabolism of 5-hydroxytryptamine and beta-phenylethylamine in perfused rat lung and in vitro.

1 Metabolism of 5-hydroxytryptamine (5-HT) and beta-phenylethylamine (PHE) by monoamine oxidase (MAO) was investigated in rat isolated lungs and in mitochondrial preparations from rat lung. 2. In perfused lungs 5-HT metabolism had an apparent Km of 2 microgram and PHE metaoblism a Km of 54 microgram, whereas in vitro the Km values were 330 microgram and 28 microgram respectively. 3 In vitro, MAO activity had substrate and inhibitor specificities compatible with the presence of A and B types of MAO. 4 In perfused lung, metabolism of 5-HT but not that of PHE was inhibited by desmethylimipramine. 5 These results show that PHE metabolism in perfused lung, unlike that of other metabolized amines, is not limited by transport and the transport process for PHE is unlike that of 5-HT or noradrenaline. 6 These results also show that the kinetic parameters obtained for MAO activity in vitro do not generally apply to the isolated lung where transport of substrate can be the deciding factor. This discrepancy emphasizes that the enzymic properties of the whole organ cannot relaibly be deduced from its enzymic content.

Animals↗
PubMed1981

Ontogenesis of uptake and deamination of 5-hydroxytryptamine, dopamine and beta-phenylethylamine in isolated perfused lung and lung homogenates from rats.

1. Uptake of 5-hydroxytryptamine (5-HT) and beta-phenylethylamine (PEA) was studied in perfused lung from male rats between 10 and 70 days old. 2. Monoamine oxidase (MAO) activity towards 5-HT, PEA and dopamine was studied in homogenate preparations of lung from rats aged between 5 and 80 days. 3. Uptake of 5-HT (10 microM) decreased throughout the age range studied but uptake of PEA (50 microM) increased for the first 30 days and beyond this age it decreased. Metabolites formed for both amines reflected the changes in uptake. 4. MAO activity deaminating 5-HT is well developed by day 10 and reaches its maximum by day 40. For dopamine and PEA, MAO activity remained low until day 20, and the developed rapidly, reaching a maximum by day 40 for dopamine; activity towards PEA did not reach a maximum by day 80. 5. These results show that uptake and MAO activity changes with age and thus the lung responds like other tissues. 6. These results also demonstrate the independent development of uptake and MAO activity towards 5-HT, PEA and dopamine.

Age Factors↗
PubMed1981

Effect of hyperoxia on uptake and metabolism of 5-hydroxytryptamine and beta-phenylethylamine in rat lung: a sex difference.

1 The uptake of 5-hydroxytryptamine (5-HT) and beta-phenylethylamine (PEA) and their deamination by monoamine oxidase (MAO) were studied in perfused lung from male and female rats exposed to 100% O(2) at 1 ATA for up to 60 h.2 The uptake and metabolism of 5-HT in lungs from both male and female rats was not changed by exposure to O(2).3 The uptake and metabolism of PEA by lungs from male rats was unchanged. Uptake of PEA by lungs from female rats was inhibited 20% and 62% after 37 h and 50 h exposure respectively.4 MAO activity, both in vitro and in perfused lung, was increased towards PEA after 35 h of hyperoxia.5 Metabolism of PEA in perfused lung, measured over 30 min, was inhibited 52% after 50 h of O(2) hyperoxia.6 These results show that exposure to high concentrations of O(2) damages lung, resulting in inhibition of uptake of PEA and consequently in inhibition of metabolism of PEA.7 These results also indicate that, in lung from female rats, MAO-type B is more susceptible to changes in O(2) tension than MAO type A.

Animals↗
PubMed1982

A pharmacological analysis of the hyperactivity syndrome induced by beta-phenylethylamine in the mouse.

1 The effects of the putative 5-hydroxytryptamine (5-HT) receptor antagonists, methysergide, mianserin and methergoline, the dopamine receptor antagonists, haloperidol, thioridazine and clozapine, and the noradrenaline (NA) receptor antagonists, phentolamine, phenoxybenzamine and propranolol on the behavioural responses of mice to beta-phenylethylamine (PEA, 75 mg/kg) have been examined.2 PEA produced a syndrome consisting of three distinct phases. The brief initial phase (0-5 min after injection) which consisted of forward walking, sniffing and headweaving, was succeeded by a locomotor depressant phase (5-20 min after injection) which consisted of abortive grooming, headweaving, splayed hindlimbs, forepaw padding, sniffing and hyperreactivity, and a late locomotor stimulant phase (20-35 min after injection), which was characterized by forward walking, sniffing, hyperreactivity, rearing and licking.3 Methysergide, mianserin, methergoline, clozapine and propranolol inhibited headweaving and splayed hindlimbs, whereas haloperidol, thioridazine, phentolamine and phenoxybenzamine had no effect on these responses. Forepaw padding was strongly inhibited by methergoline and a high dose of mianserin, and weakly antagonized by methysergide, clozapine, haloperidol and thioridazine. In contrast, padding was mildly potentiated by phenoxybenzamine and phentolamine but strongly potentiated by propranolol. It is proposed that headweaving and splayed hindlimbs are 5-HT-mediated responses whereas forepaw padding also involves 5-HT mechanisms but may be partially due to release of tryptamine.4 Rearing and licking were inhibited by haloperidol (most strongly), thioridazine and clozapine but potentiated by mianserin, methysergide, propranolol, phenoxybenzamine or phentolamine. Methergoline inhibited licking without affecting rearing. It is suggested that PEA-induced rearing and licking are produced by activation of dopaminergic neurones and inhibited by 5-HT or NA stimulation.5 Phenoxybenzamine inhibited sniffing and produced backward walking when administered prior to PEA, suggesting mediation by NA of sniffing and an inhibitory influence of NA on backward walking.6 Clozapine and thioridazine were the most effective antagonists of hyperreactivity and it is proposed that this response is dopamine-mediated. Forward walking was inhibited by high doses of haloperidol or clozapine and potentiated by methergoline, mianserin or methysergide, suggesting that hyperactivity may also be mediated by dopamine but subject to 5-HT inhibition.7 Abortive grooming was the dominant behavioural component observed after PEA administration and was prevented by all of the antagonists tested which suggests that catecholamine and 5-HT mechanisms may be involved in the expression of this response.8 Since PEA is an endogenous compound in animals and man, and has been claimed to be present in abnormal amounts in some schizophrenics, PEA-induced behavioural stimulation in mice (which includes the postulated hallucinogenic responses of abortive grooming and backward walking) may be a useful animal model of psychosis.

5-Hydroxytryptophan↗
PubMed2006

First genetic characterization of a bacterial beta-phenylethylamine biosynthetic enzyme in Enterococcus faecium RM58.

Enterococcus faecium RM58 produces beta-phenylethylamine and tyramine. A gene from Ent. faecium RM58 coding for a 625 amino-acid residues protein that shows 85% identity to Enterococcus faecalis tyrosine decarboxylase has been expressed in Escherichia coli, resulting in L-phenylalanine and L-tyrosine decarboxylase activities. Both activities were lost when a truncated protein lacking 84 amino acids at its C-terminus was expressed in E. coli. This study constitutes the first genetic characterization of a bacterial protein having L-phenylalanine decarboxylase activity and solves a long-standing question regarding the specificity of tyrosine decarboxylases in enterococci.

Carboxy-Lyases↗
PubMed1979

Phenylethylamine in paranoid chronic schizophrenia.

Phenylethylamine (PEA) is an endogenous amine that is structurally and pharmacologically related to amphetamine. Urinary PEA excretion is significantly higher in paranoid chronic schizophrenics than in nonparanoid chronic schizophrenics and normal controls. Diet, hospitalization, and medication do not account for differences in PEA concentrations. These findings offer some indication that PEA may be an endogenous amphetamine.

Chronic Disease↗
PubMed1997

Decreased beta-phenylethylamine in CSF in Parkinson's disease.

OBJECTIVE: To determine the concentrations of beta-phenylethylamine (PEA) in CSF in patients with Parkinson's disease, and to evaluate the relation between concentration of PEA in CSF and severity of Parkinson's disease. METHODS: Using gas chromatography-chemical ionisation mass spectrometry, CSF concentrations of PEA were measured in 23 patients with Parkinson's disease (mean age, 64.0 (SD 8.2) years), of whom three were at Hoehn and Yahr stage II, 11 were at stage III, and nine were at stage IV. Comparison was made with eight patients with neuropathy (mean age, 57.0 (SD 19.2) years) and 12 controls without neurological disease (mean age, 57.6 (SD 4.8) years). RESULTS: Concentrations of PEA in CSF in Parkinson's disease were significantly lower (mean 205 (SD 131) pg/ml) than in patients with peripheral neuropathy (433 (SD 254) pg/ml) and controls (387 (SD 194) pg/ml). The concentrations of PEA in CSF correlated negatively with Hoehn and Yahr stage (P<0.01). CONCLUSIONS: There are decreased CSF concentrations of PEA in patients with Parkinson's disease.

Aged↗
PubMed2001

Platelet monoamine oxidase B and plasma beta-phenylethylamine in Parkinson's disease.

OBJECTIVE: To evaluate the correlation between changes in platelet monoamine oxidase type B (MAO-B) activity and plasma beta-phenylethylamine (PEA) concentrations in patients with Parkinson's disease and controls. METHODS: Platelet MAO-B activity and plasma PEA were measured with gas chromatography-mass spectrometry (GC-MS) in patients with Parkinson's disease treated with levodopa (12 men and 12 women) or selegiline (three men and three women), and physically healthy subjects as a control group (10 men and 10 women). RESULTS: Platelet MAO-B activity was significantly higher in the Parkinson's disease group (mean 542 (SD 318) pmol/10(7) platelets/30 min) than in the control group (mean 349 (SD 307) pmol/10(7) platelets/30 min) (p<0.05). By contrast, the plasma PEA concentrations in patients with Parkinson's disease were significantly lower than in the control group (mean 532 (SD 243) pg/ml; 931 (SD 560) pg/ml) (p<0.01). The plasma PEA concentrations in patients with Parkinson's disease treated with selegiline were prominently higher than in patients with no selegiline treatment (p<0.001). There was a significantly negative correlation between platelet MAO-B activity and plasma PEA concentrations in patients (n=24, r=-0.466, p<0.001). CONCLUSIONS: The increase in platelet MAO-B activity and decrease in plasma PEA concentrations in patients with Parkinson's disease may be involved in the pathophysiological processes of the disease, and these changes are reversed by treatment with selegiline.

Aged↗
PubMed1980

Interactions between p-tyramine, m-tyramine, or beta-phenylethylamine and dopamine on single neurones in the cortex and caudate nucleus of the rat.

p-Tyramine, applied to cortical and caudate neurones with weak iontophoretic currents (0-10 nA), did not usually cause any alteration of base-line firing rate. However, neuronal responses to dopamine (DA) during such weak applications of p-tyramine were greatly enhanced. Cortical neurone responses to noradrenaline (NA) were similarly potentiated, but both cortical and caudate neurone responses to alpha-aminobutyric acid were unaffected by p-tyramine. In addition, weak background applications of DA which did not affect cell firing rate were also without effect on the neuronal responses to the standard application of DA. The responses of cortical neurones to DA were also potentiated by m-tyramine and beta-phenylethylamine applied with weak cationic currents. The results may suggest that trace amines can enhance NA and DA transmission in the central nervous system.

Action Potentials↗