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PubMed2002

Haploscleridamine, a novel tryptamine-derived alkaloid from a sponge of the order haplosclerida: an inhibitor of cathepsin K.

As part of a search for novel inhibitors of cathepsin K, the MeOH extract of a Micronesian sponge of the order Haplosclerida was shown to be active. Bioassay-guided fractionation of the extract yielded halitoxins, tryptamine, and a novel tryptamine-derived alkaloid, haploscleridamine (1). The tetrahydro-beta-carboline structure of haploscleridamine (1) was elucidated through spectral techniques. Haploscleridamine (1) was found to be an inhibitor of cathepsin K with an IC(50) of 26 microM.

Alkaloids↗
PubMed2005

Tryptamine-derived amides and alkaloids from the seeds of Annona atemoya.

A series of N-fatty acyl tryptamines, including a mixture of N-nonadecanoyltryptamine (1), N-behenoyltryptamine (2), N-lignoceroyltryptamine (3), N-cerotoyltryptamine (4), and N-octacosanoyl tryptamine (5), and a mixture of N-tricosanoyl-4,5-dihydroxytryptamine (6), N-lignoceroyl-4,5-dihydroxytryptamine (7), N-pentacosanoyl-4,5-dihydroxytryptamine (8), and N-heptacosanoyl-4,5-dihydroxytryptamine (9), along with two alkaloids, atemoine (10) and cleistopholine, were isolated from the EtOAc extract of seeds of Annona atemoya. The structures of the new compounds, 1 and 5-10, were determined on the basis of spectral evidence.

Alkaloids↗
PubMed2001

A putative metabolite of serotonin, tryptamine-4,5-dione, is an irreversible inhibitor of tryptophan hydroxylase: possible relevance to the serotonergic neurotoxicity of methamphetamine.

Tryptamine-4,5-dione (T-4,5-D) is formed as a result of oxidation of 5-hydroxytryptamine by superoxide (O(2)(-)(*), nitric oxide (NO*), and peroxynitrite (ONOO(-)). T-4,5-D rapidly inactivates tryptophan hydroxylase (TPH), derived from rat brain, probably as a result of covalent modification of active site cysteine residues. The activity of TPH exposed to T-4,5-D cannot be restored by anaerobic reduction with dithiothreitol (DTT) and ferrous iron (Fe(2+)) indicating that the inactivation is irreversible. 7-S-Glutathionyl-tryptamine-4,5-dione, formed by the rapid reaction between T-4,5-D and glutathione, also inhibits TPH but in this case the activity is restored by anaerobic reduction with DTT/Fe(2+). The results of this investigation may be relevant to the initial reversible and subsequent irreversible inactivation of TPH evoked by methamphetamine and 3,4-methylenedioxymethamphetamine.

Animals↗
PubMed2003

Determination of the amino acid tryptophan and the biogenic amine tryptamine in foods by the heavy atom induced-room temperature phosphorescence methodology.

Very simple and selective methods are presented to determine the amino acid tryptophan (Trp) and the biogenic amine tryptamine (Tryp), both compounds with an indole-type molecular structure by the methodology named Heavy Atom Induced-Room Temperature Phosphorescence (HAI-RTP) which constitutes the first time that HAI-RTP has been used to detect compounds with non-naphthalenic structures in their molecules. Different variables affecting the phosphorescence signal (heavy atom perturber and sodium sulfite concentration) were carefully studied. The analytical curves give a linear dynamic range of 15-100 ng ml(-1) and a detection limit of 4 ng ml(-1) for Trp and 94-400 ng ml(-1) and 28 ng ml(-1) for Tryp. The methods have been successfully applied to the analysis of complex food matrices such as the presence of tryptophan in yoghurt and tryptamine in bottled beer. A single alkaline hydrolysis to release Trp from yoghurt proteins and two methods for extracting Tryp from beer samples are proposed and optimised. A total Trp content of 374 mg of Trp per kg of yoghurt was quantified by the standard addition method of calibration and a recovery of 90% was obtained for 250 ng ml(-1) of Tryp in spiked non-alcoholic beer samples.

Beer↗
PubMed1981

Comparison of the contraction produced by various tryptamine analogues on human basilar arterial and rat aortic strips in vitro.

The effect of various closely related analogues of 5-hydroxytryptamine were studied on the human basilar arterial and rat aortic strips in vitro. All analogues (except 5-methoxytryptamine) contracted both preparations producing maximal responses equivalent to that obtained with 5-hydroxytryptamine. Maximum responses to 5-methoxytryptamine were equivalent to and only 60% of the maximum obtained with 5-hydroxytryptamine on human basilar artery and rat aorta, respectively. The order of potency of the analogues on the human basilar artery was different from that obtained on the rat aorta. 5-methyltryptamine, N-methyltryptamine and tryptamine were equipotent on both tissues, whereas 5-hydroxytryptamine and 5-methoxytryptamine were 229 and 296 times more potent, respectively, on the human basilar artery compared to the rat aorta. Both tissues appear to be deficient in monoamine oxidase, since nialamide or iproniazid did not potentiate responses to tryptamine. It is concluded that the receptor type mediating contraction of the human basilar artery to 5-hydroxytryptamine is different from the classical smooth muscle D-receptor.

5-Methoxytryptamine↗
PubMed2002

Melatonin, serotonin, and tryptamine in some egyptian food and medicinal plants.

The mammalian pineal hormone melatonin (N-acetyl-5-methoxytryptamine), an aminoindole produced by the metabolism of serotonin (5-hydroxytryptamine), has been shown to be a potent scavenger for the highly toxic hydroxyl radical. Three substances that are very important in animal physiology (e.g., in brain metabolism) are noradrenaline, histamine, and serotonin; all three occur in plants. Here we report that serotonin, tryptamine, and melatonin were found in some edible and medicinal plants in Egypt. The results of this screening showed that the pulp of underripe and ripe yellow banana contains 5-hydroxytryptamine at concentrations of 31.4 and 18.5 ng/g, respectively. Corn, rice, barley grains, and ginger showed the highest concentrations of melatonin, at 187.8, 149.8, 87.3, 142.3 ng/100 g, respectively. On the other hand, potato samples were free from all indolamines. Pomegranate and strawberry showed a low level of indolamines (8-12 microg/g serotonin, 4-9 microg/g tryptamine, and 13-29 ng/100 g melatonin).

Food Analysis↗
PubMed1994

Immunocytochemical localization of tryptamine in the rat brain.

Immunocytochemical localization of tryptamine in rat brain was performed at light and electron microscope level. The immunoreactive cells were present in the mesencephalon, pons and medulla, around the interpendicular nucleus in the reticular substantia nigra and in the giganto cellularis ventralis nucleus. Immunoreactive fibres were present in the dorsal region of the brain stem, and innervated the hippocampus, the ependymal epithelium and the corpus striatum. An ultrastructural study revealed that tryptamine was present only in neuronal perikaryon and processes.

Animals↗
PubMed2005

Crystallization and preliminary X-ray analysis of strictosidine synthase and its complex with the substrate tryptamine.

Strictosidine synthase (STR1) is a central enzyme that participates in the biosynthesis of almost all plant monoterpenoid indole alkaloids. After heterologous expression in Escherichia coli, crystals of STR1 and its substrate complex with tryptamine were obtained by the hanging-drop technique at 302-304 K with potassium sodium tartrate tetrahydrate as precipitant. All crystals belong to space group R3. The native STR1 crystals diffract to 2.95 A and have unit-cell parameters a = b = 150.3, c = 122.4 A. The tryptamine complex crystals diffract to 2.38 A, with unit-cell parameters a = b = 147.3, c = 122.3 A.

Carbon-Nitrogen Lyases↗
PubMed1988

Formation of a new biogenic aldehyde adduct by incubation of tryptamine with rat brain tissue.

Tryptamine was degraded by incubation with rat brain homogenate to an unknown product. The reaction was stimulated by the nonionic detergents Triton X-100 and Lubrol PX and less by the zwitterionic detergent 3-[(3-cholamidopropyl)dimethylammonio]1-propanesulfonate (CHAPS). The same results were obtained with pig brain and bovine brain. The monoamine oxidase inhibitor pargyline inhibited the reaction strongly, indicating the participation of the enzyme on the reaction. Addition of 17,000 g supernatant from rat brain homogenate increased the formation effectively whereas phospholipids or chloroform/methanol (7:3) extract from the 17,000 g supernatant showed only little or no effect. Chromatographic and electrophoretic properties as well as the chemical reaction of the product with specific reagents suggest that the compound consists of an indole part and an amino acid part. The product could be identified by fast atom bombardment mass spectrometry and by comparison with the synthetic substance (4R)-2-(3-indolylmethyl)-1,3-thiazolidine-4-carboxylic acid. It is formed by the enzymatic oxidation of tryptamine producing indole-3-acetaldehyde which spontaneously cyclizes with free L-cysteine from the tissue. The results suggest that the reaction of biogenic aldehydes with brain macromolecules may proceed via an analogous reaction.

Acetaldehyde↗
PubMed1974

Effect of ethanol on the oxidative metabolism of tryptamine by rat liver homogenate.

1 The effect of a wide range of ethanol concentrations (v/v) on indoleacetic acid (IAA) formation from the oxidative deamination of tryptamine was studied in vitro, in rat whole liver homogenate.2 IAA production was inhibited progressively by ethanol in concentrations between 0.01% to 0.2%, but the inhibition declined when the ethanol concentration was increased further to 6%.3 Ethanol-induced inhibition of IAA formation was only partially reversed by excess aldehyde dehydrogenase, whereas reductions in IAA formation were completely prevented by pyrazole or ethanol (6% and 10%) itself.4 Excess nicotinamide adenine dinucleotide failed to alter the inhibitory effect of ethanol and no evidence was obtained for inhibition of monoamine oxidase by ethanol or its metabolite, acetaldehyde.5 We conclude that ethanol indirectly inhibits IAA production as a result of oxidation of ethanol by alcohol dehydrogenase, during which the oxidative metabolism of tryptamine is shifted towards the reductive pathway, thus favouring the formation of tryptophol in place of IAA.

Acetaldehyde↗
PubMed1974

Indoleamine antagonists: relative potencies as inhibitors of tryptamine- and 5-hydroxytryptophan-evoked responses.

Four indoleamine antagonists were evaluated for relative potencies as inhibitors of tryptamine-induced forepaw clonus and 5-hydroxytryptophan-evoked head twitches. Methergoline was approximately three times more potent against the forepaw clonus than the head twitch response, whereas methysergide exhibited nearly equal activity in both tests. Cyproheptadine and cinanserin showed a profile opposite to methergoline and a greater degree of selectivity, being 25 to 40 times more potent as inhibitors of the 5-hydroxytryptophan- than of the tryptamine-induced response. These findings clearly demonstrate that the rank order of potency of indoleamine antagonists varies greatly depending upon the test procedure employed.

5-Hydroxytryptophan↗
PubMed1974

Further studies on the mode of action of psychotomimetic drugs: antagonism of the excitatory actions of 5-hydroxytryptamine by methylated derivatives of tryptamine.

1 The actions of 5-methoxytryptamine (5-MeOT), N,N-dimethyltryptamine (DMT), 5-hydroxy-N,N-dimethyltryptamine (bufotenine, 5-HODMT) and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT), and their interactions with 5-hydroxytryptamine (5-HT), acetylcholine, (-)-noradrenaline, and glutamate were studied by microiontophoresis on single neurones in the brain stem of rats anaesthetized with urethane or decerebrate cats.2 Like D-lysergic acid diethylamide (LSD 25) the three psychotomimetic derivatives (DMT, 5-HODMT, 5-MeODMT) specifically antagonized 5-HT excitations of single neurones, but the non-psychotomimetic 5-MeOT had no antagonistic effects.3 In contrast to LSD 25, the psychotomimetic tryptamines only rarely antagonized glutamate effects, indicating that the excitatory 5-HT receptors and the glutamate receptors on the same neurones may be closely related spatially, but are separate.4 The methylated tryptamine derivatives were able to mimic the actions of 5-HT on neurones. The non-psychotomimetic 5-MeOT was most potent in this respect, while the other three derivatives which are psychotomimetic, were less active.5 The 5-HT mimicking actions of 5-MeOT were the same in rats pretreated with p-chlorophenylalanine or reserpine as in untreated rats. It therefore seems that the 5-HT mimicking actions are unlikely to be due to release of 5-HT, but are due to direct actions on 5-HT receptors.6 The evidence presented supports the hypothesis that LSD-like psychotomimetics act by an antagonism of 5-HT in the lower brain stem, and is not compatible with the suggestion that the psychotomimetic action of these drugs is related to 5-HT receptor stimulation.

Acetylcholine↗
PubMed1976

Pressor effects of tryptamine analogues.

1. Methylation of tryptamine in the 1-position had little effect on the potency of the drug as a pressor agent in the intact anaesthetized rat. 2. In contrast, substitution of a benzo[b]thiophene ring system for the indole ring decreased the pressor activity. 3. Pretreatment of the animals with reserpine reduced the pressor effect of tryptamine and its benzo[b]thiophene analogue while increasing the effect of the 1-methylindole analogue. 4. Pretreatment with phenoxybenzamine reduced the pressor effect of all three compounds.

Animals↗
PubMed1987

Differential classification of vascular smooth muscle and endothelial cell 5-HT receptors by use of tryptamine analogues.

In ring preparations of the rabbit external jugular vein contracted with the thromboxane-mimetic U-46619, submicromolar concentrations of 5-hydroxytryptamine (5-HT) and chemically related analogues produced relaxations that were dependent on the integrity of the vascular endothelium. The receptor mediating endothelium-dependent relaxations was evidently similar to previously described endothelial 5-HT receptors since relaxation responses to alpha-methyl-5-HT were not blocked by atropine, (+/-)-propranolol, yohimbine, indomethacin, ketanserin or MDL-72222, but were non-competitively antagonized by methysergide, methiothepin and cyproheptadine. The activities of some tryptamine agonists and antagonists at the endothelial 5-HT receptor in rabbit jugular vein were compared with their activities at the smooth muscle 5-HT2-receptor in rabbit aortic rings. Differences in the tryptamines' affinities and relative efficacies showed that the endothelial 5-HT receptor was not of the 5-HT2-type. The high agonist potencies of 5-HT and 5-carboxamidotryptamine, the susceptibility to antagonism by both methiothepin and methysergide and the resistance to blockade by selective 5-HT2 and 5-HT3 ('M') receptor antagonists implies that the endothelial receptor belongs to the '5-HT1-like' class. However, the agonist potency order 5-HT = alpha-methyl-5-HT greater than 5-carboxamidotryptamine suggested that the receptor is not the same as the peripheral '5-HT1-like' receptors reported to mediate directly contraction of the dog saphenous vein or relaxation of vascular and non-vascular smooth muscles. At these receptors, the potency order is 5-carboxamidotryptamine greater than 5-HT greater than alpha-methyl-5-HT. These results constitute preliminary evidence that peripheral '5-HT1-like' receptors, like central 5-HT1 recognition sites, are a heterogeneous population. Further comparative studies with a wider range of receptor probes are necessary to establish whether or not these receptors represent functional counterparts of the ligand binding sites in the brain.

Animals↗
PubMed1980

Tetrahydro-beta-carbolines and corresponding tryptamines: In vitro inhibition of serotonin, dopamine and noradrenaline uptake in rat brain synaptosomes.

The structure activity relationships of tryptolines and some other beta-carbolines and tryptamines as inhibitors of serotonin (5-HT), dopamine (DA) and noradrenaline (NA) uptake were studied in rat brain synaptosomes. All beta-carbolines inhibited to higher degree the uptake of 5-HT than that of DA or NA(IC50's 5-100 times lower). The most potent tryptoline derivative was 6-hydroxy-tetrahydro-beta-carboline (5-hydroxytryptoline, 6-OH-THBC) with an IC50 of 5.0 x 10(-7) M at a 5-HT concentration of 10(-7) M. 6-Methoxy-tetrahydro-beta-carboline (5-methoxytryptoline) was slightly weaker; the inhibition of 5-HT uptake and DA uptake being competitive. Also tetrahydro-beta-carboline (tryptoline) was more potent than its 1-methylderivative, tetrahydroharmane (methtryptoline) or norharmane (beta-carboline). All of them were, however, weaker inhibitors of 5-HT uptake than the freely rotating indoleamines N-methyl-tryptamine (N-Me-T) or 5-HT itself. N-Me-T and 5-HT were also more potent inhibitors of DA and NA uptake than most of the beta-carbolines, DA uptake, however, was inhibited better by 6-OH-THBC than by 5-HT or N-ME-T. Tetrahydro-beta-carbolines may inhibit 5-HT uptake also in vivo but is unlikely that catecholamine uptake is affected.

Animals↗
PubMed1980

Tetrahydro-beta-carbolines and corresponding tryptamines: In vitro inhibition of serotonin and dopamine uptake by human blood platelets.

Tetrahydro-beta-carbolines (THBCs), 6-methoxyharmalan and norharman and the corresponding open chain tryptamines studied inhibited t-hydroxytrypere better inhibitors of DA than 5-HT uptake but THBCs generally were far more potent inhibitors of 5-HT uptake than of DA uptake. 6-methoxy-1,2,3,4-tetrahydro-beta-carboline was as potent as 5-HT itself 3H-5-HT uptake inhibition in platelets and the inhibition was competitive. All the beta-carbolines studied were more potent inhibitors of 3h-da uptake than DA itself. Contrary to results in rat brain synaptosomes, THBCs were more potent in platelets than the corresponding tryptamines with the freely rotating ethylamine side chain. Unsaturated beta-carbolines were weaker inhibitors than THBCs. The clear difference in the rank order of potencies of these compounds in human platelets and rat brain synaptosomes demonstrates that these different model systems for amine uptake studies do not always give comparable results. The results also suggest that there are differences in the uptake systems for 5-HT and DA in human platelets.

Blood Platelets↗
PubMed1994

Interactions of monoamine oxidase inhibitors, N-acetylenic analogues of tryptamine, with rat liver microsomal cytochrome P450.

Interactions between some novel and potent monoamine oxidase inhibitors (MAOIs), acetylenic analogues of tryptamine, and rat liver microsomal cytochrome P450 (P450) as evidenced by visible spectra analysis were analysed. Compounds with a secondary aliphatic amine moiety throughout induced type II difference spectra and exhibited the highest affinity for P450, whereas tertiary amines induced type I spectral changes and showed diminished affinity. P450 dependent aniline hydroxylase activity was inhibited by all compounds in an irreversible time-dependent manner. Only tertiary aliphatic amines constituted the substrate for P450-dependent N-demethylase activity, with comparable kinetic parameters. The N-demethylated metabolites were identified by thin-layer chromatography and mass-spectrometric analyses. These findings describe the role of P450-dependent microsomal mono-oxygenase systems in the metabolism of some MAOI acetylenic tryptamine derivatives and the possible hepatic contribution to adverse interactions between MAOIs, endobiotics and sympathomimetic compounds.

Acetylene↗
PubMed1982

Stability of Lambdoid bacteriophage heads: antagonism between polyamines and tryptamine.

The biological activity of heads of bacteriophages phi 80 and lambda in in vitro assembly with tails was inhibited by dialysis, filtration on gels, and treatment with tryptamine. Inhibition by these three treatments could be prevented but not reversed by putrescine. Other diamines with shorter or longer carbon chain lengths were either less effective or not effective at all. It is suggested that tryptamine acts by loosening the tightly packed DNA in heads, whereas putrescine stabilizes it.

Bacteriophage lambda↗