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At least 19 recordsLinked to original sources
PubMed1978

[Relations between urinary 3-methoxytyramine and the peripheral metabolism of dopamine in human adults and children].

3-Methoxytyramine (3-MT), the direct metabolite of dopamine (DA) is present in human urines at birth. The rate of its urinary excretion (microgram/24 h) increases highly from birth to 12 months of age; in the next period of infancy, the increase is slower and parallel to that of creatininury; after 15 years, the urinary amounts of 3-MT remain nearly constant, with advancing age. The analysis of the possible sources of urinary 3-MT, lead us to suggest that this compound has essentially a peripheral origin. On the other hand the comparison between urinary data of 3-MT and DA in normal infants and adult subjects has shown that 3-MT excretion is less affected by dietary input than DA itself, so that it can be concluded that urinary 3-MT is a better indication of peripheral dopaminergic activity than urinary DA, chiefly in the young child.

Adolescent↗
PubMed1979

An improved method for the differential assay of 3-O-methylated catecholamines in human urine using ion-pair extraction and gas chromatography electron capture detection.

A gas chromatographic method is described for the quantitative determination of urinary normetadrenaline, metadrenaline and 3-methoxytyramine using electron capture detection. The N,O-dipentafluoropropionyl beta-O-ethyl derivatives of normetadrenaline and metadrenaline and the N,O-dipentafluoropropionyl derivative of 3-methoxytyramine were prepared. The amines were purified by ion exchange chromatography and ion pair extraction. Amine derivatives from urine extracts were identified definitively by mass fragmentography. The 24-h excretion value for normetadrenaline in human urine is 167 +/- 95 micrograms (mean +/- S.D.), for metadrenaline is 116 +/- 74 micrograms (mean +/- S.D.) and for 3-methoxytyramine is 82 +/- 68 micrograms (mean +/- S.D.).

Catecholamines↗
PubMed2026

Metabolomics-based authentication of acacia honey against C3 and C4 sugar adulteration.

Acacia (Robinia pseudoacacia) honey is frequently adulterated with low-cost alternatives via direct syrup addition or in-hive sugar feeding. We focused on sugar-feeding adulterants, which is difficult to distinguish from nectar-based honey. Stable carbon isotope ratio analysis (SCIRA) is an established method for assessing honey authentication; however, its applicability is limited to detecting C4 plant-derived sugar adulteration. Therefore, we developed a metabolomics-based multi-marker strategy to discriminate acacia honey from beet-sugar (C3)- and cane-sugar (C4)-fed honey. Thirteen metabolites were prioritized using combined multivariate and univariate criteria. Subsequently, 1716 panels of seven-marker (13C7) were evaluated for discrimination performance. 291 panels achieved 100% accuracy in an independent validation set. In blending scenarios, acacia honeys spiked with 20% beet-sugar-fed honey and 20% cane-sugar-fed honey were successfully identified, outperforming SCIRA (60%) and beet-sugar marker 3-methoxytyramine (3-MT) (30%). These findings establish metabolomic panels as a robust marker for acacia honey authentication, extending beyond current reference methods.

Acacia↗
PubMed1979

Age-related changes in catecholamine metabolites of human urine from birth to adulthood.

Catecholamines (dopamine [DA], norepinephrine [NE], epinephrine [E]), methoxyamines (3-methoxytyramine [MT], normetanephrine [NMN], metanephrine [MN]), DOPA, and acidic metabolites (3,4-dihydroxyphenylacetic acid [DOPAC], vanilmandelic acid [VMA]) were determined in human urines from one day of age to adulthood, in order to investigate sympatho-adrenal development during life. All adrenergic compounds are present in neonate urines on the first day of life, but their postnatal evolution is quite different according to the nature of metabolites. Daily E, MN and VMA amounts remain low until the 10th month of life; daily NE, MT and DOPA levels increase progressively, but, in contrast, NMN amounts are already high in the neonatal period and increase only beyond the fourth year of age. DA is at either age the predominant catecholamine but its elimination is relatively more important in the neonatal period.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1977

Interaction of haloperidol and gamma-butyrolactone with (+)-amphetamine-induced changes in monoamine synthesis and metabolism in rat brain.

The interaction of (+)-amphetamine with haloperidol and gamma-butyrolactone on synthesis of monoamines in rat brain regions was investigated using an in vivo method, in which the accumulation of dopa and 5-hydroxytryptophan (5-HTP) was measured after inhibition of the aromatic amino acid decarboxylase by means of 3-hydroxybenzylhydrazine. The accumulation of 3-methoxytyramine (3-MT) after inhibition of the monoamine oxidase with pargyline was taken as an indicator of the in vivo release of dopamine (DA) into the extraneuronal space. (+)-Amphetamine at doses of 1--3 mg/kg caused an increase of dopa formation in the DA-rich areas c. striatum and mesolimbic forebrain but had no effect on dopa formation in neocortex and 5-HTP formation in all brain regions investigated. At a dose of 10 mg/kg (+)-amphetamine decreased dopa as well as 5-HTP formation in all brain regions studied. 3-MT accumulation in whole rat brain was stimulated by (+)-amphetamine as well as haloperidol and inhibited by gamma-butyrolactone. Combined treatment with haloperidol and (+)-amphetamine not only potentiated the stimulation of dopa formation but also the increase of 3-MT accumulation. Pretreatment with gamma-butyrolactone antagonized the stimulation of 3-MT formation induced by (+)-amphetamine at a dose of 10 mg/kg. This dose of (+)-amphetamine markedly counteracted the gamma-butyrolactone-induced increase in dopa formation especially in the DA-rich areas. The data support the view that impulse flow in DA neurons facilitates the effect of (+)-amphetamine on DA release and DA synthesis. Inhibition of catecholamine synthesis after high doses of (+)-amphetamine may be due to an increase in cytoplasmatic DA concentration causing end-product inhibition of tyrosine hydroxylase.

4-Butyrolactone↗
PubMed1976

Effects of chemical stimulation of the mesolimbic dopamine system upon locomotor activity.

The effects of local injections of drugs into terminal areas of the mesolimbic dopamine system were investigated. Bilateral administration of dopamine, but not of noradrenaline and serotonin, into the nucleus accumbens of non-pretreated rats resulted in stimulation of locomotor activity. No clear or only minor effects were seen after injections of the dopamine metabolites 3-methoxytyramine, DOPAC and HVA and after injections of media with different pH and osmolality. d-Amphetamine proved more effective than dopamine in producing locomotor stimulation, whereas both stimulant and depressant effects were observed following injection of apomorphine into the nucleus accumbens. ET 495 and the noradrenaline agonists clonidine, phenylephrine and isoprenaline did not enhance locomotor activity, but theophylline was effective. Pretreatment with haloperidol, but not with clozapine, significantly reduced the effects of dopamine and theophylline. Locomotor stimulation was also found following bilateral administration of dopamine, d-amphetamine and apomorphine into the tuberculum olfactorium, whereas noradrenaline, serotonin and ET 495 produced no, or rather depressant effects. These results provide further evidence for an important role of the mesolimbic dopamine system with respect to locomotor activity.

Animals↗
PubMed1977

Changes in striatal dopamine metabolism during precipitated morphine withdrawal.

Precipitation of withdrawal in morphine tolerant/dependent rats by either naloxone or the partial agonist ZK 48491 caused a significant increase in the contration of striatal DA, which persisted for at least 1 h. During the same time the probenecid-induced accumulation of HVA and DOPAC was reduced in the striatum in relation to probenecid-treated tolerant/dependent controls. 20 min after precipitation of withdrawal by naloxone, the striatal concentration of 3-methoxytyramine was decreased by about 40%, while the activity of the DA metabolizing enzymes, MAO and COMT, remained unchanged. Naloxone-precipitated withdrawal was, further, found to delay the depletion of striatal DA caused by inhibition of synthesis 90 min after alpha-methyl-p-tyrosine treatment. All these results provide evidence for a decreased release of DA from the striatum during precipitated morphine withdrawal.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1977

Potentiating effect of lithium chloride on methamphetamine-induced stereotypy in mice.

Single administration of LiCl potentiated the methamphetamine-induced stereotypy in mice, without affecting the concentration of methamphetamine in brain. During MAO inhibition, the level of 3-methoxytyramine (3-MT), an O-methylated metabolite of dopamine, was reduced by LiCl, but the elevated 3-MT level observed after the administration of methamphetamine was not influenced by LiCl.

Animals↗
PubMed2026

An Integrative Proteomic Approach to Reveal Altered Signaling Modules During Alzheimer's Disease Progression in PS19 Tauopathy Mice.

Alzheimer's disease (AD) is a slowly progressive neurodegenerative disease that is characterized by cognitive, functional, and behavioral impairments. These changes occur owing to the progressive accumulation of extracellular amyloid-beta plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau protein. AD is associated with the dysfunction of several essential neurotransmitter systems, such as dopamine, and impaired neurotransmission. Despite the association of neurotransmitter changes within the brain and AD pathology, in-depth profiling studies on neurotransmitters and their related proteomic changes are limited. This study was conducted to profile and integrate the proteomes and neurotransmitters in seven brain regions of PS19 (Tau P301S) mice according to AD progression between 4 and 7 months. Proteomic analysis revealed significantly altered canonical pathways in various brain regions, including metabolic abnormalities. In the neurotransmitter profile, we found significant alterations in the levels of six neurotransmitters-dopamine, serotonin, homovanillic acid, norepinephrine, 3-methoxytyramine, and 3,4-dihydroxyphenylacetic acid-during AD progression. Using an integrative approach between proteome and neurotransmitter profiles, we found that AD progression-dependent dopamine- and serotonin-related signaling modules are closely related to neurotransmitter changes, especially in the hippocampus and cerebellum. This integrative approach could provide new signaling modules to help understand AD progression and thereby enable improved treatment and clinical outcomes.

Animals↗
PubMed1977

Conjugated catechol derivatives in a transplantable islet cell tumour of the golden hamster.

Two glucuronidated catechol have been identified in a transplantable islet cell tumour of the golden hamster, i.e. dopamine-4-O-glucuronide and 3-methoxytyramine-4-O-glucuronide. L-dopa is rapidly metabolized in the tumour to one or both of these glucuronides. Incubation of tumour homogenates in the presence of beta-glucuronidase shows that dopamine-4-O-glucuronide is present in the tumour in extremely high concentrations.

Adenoma, Islet Cell↗
PubMed1975

Dopamine induced relaxation of isolated canine renal, mesenteric, and femoral arteries contracted with prostaglandin F2-alpha.

The purpose of this investigation was to develop a system for studying the effects of dopamine on isolated blood vessels. Canine renal, mesenteric, and small femoral arteries (less than 1 mm outside diameter) were exposed to phenoxybenzamine 10-5 M for one hour and contracted with prostaglandin F2-alpha. Cumulative concentrations of dopamine ranging from 10-6 to 10-4 M caused dose-related relaxation of the arteries. Propranolol 10-6 M did not affect the relaxation in concentrations which markedly antagonized the effects of isoproterenol. Large femoral arteries (greater than 1 mm outside diameter) did not relax with similar concentrations of dopamine. N-methyldopamine (epinine) produced similar relaxation; 3-methoxytyramine was inactive. Specific antagonism could not be demonstrated by the postulated dopamine antagonists-haloperidol, chlorpromazine, apomorphine, or bulbocapnine-in concentrations up to 10-5 M. Higher concentration of these agents could not be used because they caused the arteries to relax. This study demonstrated that PGF2-alpha-contracted arteries pretreated with phenoxybenzamine are suitable for further investigations of putative dopamine agonists and antagonists.

Adrenergic beta-Antagonists↗
PubMed2026

Biomarkers of metastatic disease in pheochromocytoma and paraganglioma.

Pheochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumors with variable metastatic potential. While metastatic disease occurs in approximately 10-20% of cases, its prediction remains a major clinical challenge, as no histological system has been universally validated to reliably identify aggressive tumors at diagnosis. This review aims to provide a comprehensive and updated overview of current and emerging biomarkers of metastatic risk in PPGL, encompassing histopathological scoring systems, genetic and molecular markers, biochemical phenotyping, liquid biopsy approaches, and imaging-based biomarkers. Among established markers, germline SDHB mutation status, loss of SDHB expression by immunohistochemistry, elevated plasma 3-methoxytyramine, and histopathological scoring systems, such as GAPP and COPPS, represent the most clinically validated tools for risk stratification. Emerging biomarkers - including somatic alterations in ATRX and TERT, genomic instability indices, tumor immune microenvironment characterization, circulating tumor DNA, and oncometabolite quantification - show promise in refining prognostic assessment but require prospective validation before routine clinical implementation. Accurate risk stratification in PPGL demands a multiparametric and dynamic approach, integrating clinical, genetic, biochemical, and molecular parameters. Future progress will depend on large prospective international cohorts, standardized biomarker platforms, and biomarker-driven clinical trial designs to translate emerging molecular knowledge into improved patient outcomes.

SDHB↗
PubMed1979

[Effects of precursors and metabolites of catecholamines on motricity of isolated rat duodenum. Particular reference to dopamine].

Studying the effects, on the isolated rat duodenum motricity, of ten compounds precursors or metabolites of catecholamines, the following results were obtained: The direct metabolites of epinephrine and norepinephrine (metanephrine, normetanephrine), are either ineffective at concentrations below 5 X 10(-6) M, or weakly inhibitory at higher concentrations. Such inhibitory effects are prevented by alpha- and beta-blockers. 3-methoxy, 4-hydroxyphenylglycol and vanylmandelic acid have no significant effect. The catecholamine precursor, dopamine, the related compounds DOPA, 3 methoxytyramine, and to a lesser extent, 3-O methyl DOPA and homovanillic acid, have excito-motor effects at concentrations ranging mainly from 10(-7) M to 10(-5) M. At higher concentrations, the same compounds frequently exhibit inhibitory effects. The excito-motor effects might be due to a serotoninergic mechanism, since they are suppressed by the serotoninergic blocking agents methysergide and cyproheptadine. Furthermore, in the case of DOPA, we were able to establish a relationship between the excito-motor effects and duodenal serotonin stores. As for the inhibitory effects, they may be prevented by using alpha and beta blocking agents. Dihydroxyphenylacetic acid has no effect on the isolated rat duodenum motricity. The fact that dopamine and related compounds may have excitomotor effects at some concentrations, correlated with some physiopathological observations in man and animal allows some considerations about the eventual role of dopamine on intestinal motricity.

Animals↗
PubMed1979

Determination of catecholamines and their 3-O-methylated metabolites in urine by mass fragmentography with use of deuterated internal standards.

We report the determination of catecholamines (dopamine, norepinephrine, and epinephrine) and their 3-O-methylated metabolites (3-methoxytyramine, normetanephrine, and metanephrine) in urine by gas chromatography/mass spectrometry, with use of stable isotopically labeled internal standards. Normal excretion values in terms of creatinine, expressed as a function of age, are given, together with results obtained for patients with neuroblastoma, ganglioneuroblastoma, pheochromocytoma, parkinsonism treated with L-DOPA plus peripheral decarboxylase inhibitor, and a patient with cardiogenic shock treated with dopamine. The results obtained for normal adults are discussed in relation to other catecholamine metabolites and mean overall catecholamine turnover.

Adolescent↗
PubMed1977

Demethylation of O-methyl metabolites of catecholamines in erythrocytes: a methanol-forming reaction.

When lysates of erythrocytes of 11 species, including man, were incubated at pH 7.8 with L-3-methoxy-4-hydroxy [U-14C]phenylalanine or with [7-3H]normetanephrine, these were demethylated and formed 3,4-dihydroxy[14C]phenylalanine or [3H]norepinephrine. These catechols were identified by column and paper chromatographic methods. When [14C-methoxy]normetanephrine was incubated with lysates of rat erythrocytes, the one-carbon product was identified as [14C]methanol by the isolation in the incubation mixture of [14C]methanol-3,5-dinitrobenzoate and its recrystallization to constant specific radioactivity. Metanephrine, 3-methoxytyramine, vanilmandelic acid, and 3-methoxy-4-hydroxyphenylglycol were also O-demethylated by rat erythrocytes; epinephrine was not N-demethylated. The reaction was not influenced by the addition of S-adenosylmethionine. The reaction appears to be different from that catalyzed by the "methanol-forming enzyme" previously described in erythrocytes and in other tissues.

Animals↗