Disease relevance of Methoxytyramine

• Biochemical and clinical manifestations of dopamine-producing paragangliomas: utility of plasma methoxytyramine [1].
• Measurements of plasma-free methoxytyramine, in addition to normetanephrine and metanephrine, are unlikely to improve diagnosis of pheochromocytomas in hypertensive patients with symptoms of catecholamine excess but may be useful in selected patients for identification of tumors that produce predominantly dopamine [1].
• The 3-methoxytyramine concentrations in the brains of animals killed by decapitation or by microwave irradiation were compared [2].
• 3-Methoxytyramine excretion normalized when cholestasis resolved [3].
• Urinary excretion of dopa and 3-methoxytyramine but not of other catecholamine metabolites was elevated during cholestatic liver disease [3].

Psychiatry related information on Methoxytyramine

• During flashbacks, plasma norepinephrine levels increased, and the flashbackers, 11 of whom had experienced stressful events plus frightening psychotic symptoms, had an additional small increase in plasma levels of 3-methoxytyramine, which is indicative of dopamine release [4].
• Ten minutes after systemic administration, morphine at 1.25 mg/kg decreased locomotor activity and the levels of 3-methoxytyramine (3-MT), whereas at 20 mg/kg locomotor activity and 3-MT levels increased [5].
• The results suggest that monitering urinary dopamine and 3-methoxytyramine excretion in Tourette's disease may predict the clinical response to pharmacotherapy, and that a dopaminergic mechanism may be associated with this type of motor hyperkinesia [6].

High impact information on Methoxytyramine

• Methylation by catechol-O-methyltransferase did not appear to play a major role in the inactivation of tissue catecholamines since there were no noticeable increases of normetanephrine or 3-methoxytyramine in the tissues of the rats with pheochromocytoma [7].
• We normalized values for urinary 24-h excretion of metanephrine, normetanephrine, and 3-methoxytyramine by dividing by an age- and sex-specific reference range [8].
• However, in the substantia nigra, the addition of pargyline to reserpine resulted in dopamine concentrations as high as after pargyline only and the 3-methoxytyramine accumulation was not changed compared with pargyline-treated controls [9].
• This study was undertaken, using microdialysis, to compare the extracellular concentration of 3-methoxytyramine and dopamine in dialysate from the striatum and substantia nigra, after pargyline (75 mg/kg), after pargyline plus amphetamine (3 mg/kg), and after pargyline plus reserpine (5 mg/kg) administration [9].
• In the 6-hydroxydopamine-lesioned rats, levels of dopamine and its metabolites homovanillic acid, 3,4-dihydroxyphenylacetic acid, and 3-methoxytyramine were decreased, as expected, in cortex and neostriatum, but remained unmodified in thalamus [10].

Chemical compound and disease context of Methoxytyramine

• Dialysate serotonin and 3-methoxytyramine concentrations were below detection limits except for samples collected during ischemia and early reperfusion [11].
• Both the free and the conjugated forms of DA, MT, and DOPAC were increased by hypoxia [12].

Biological context of Methoxytyramine

• Enhanced 3-methoxytyramine levels in crown gall tumours and other undifferentiated plant tissues [13].
• Large deviations from Michaelis-Menten kinetics are also observed when 3-methoxytyramine is used as acyl acceptor [14].
• The incubation of brain, liver and kidney homogenates with 3-OM-L-DOPA (5 mM) did not result in the formation of 3-methoxytyramine, the compound expected to result from the decarboxylation of 3-OM-L-DOPA [15].
• Extractive acylation and mass spectrometric assay of 3-methoxytyramine, normetanephrine, and metanephrine in cerebrospinal fluid [16].
• The stabilities of 3,4-dihydroxybenzylamine (DHBA), dopamine, 3-methoxytyramine, normetanephrine and metanephrine standards under acid, base and enzymatic hydrolysis conditions were studied [17].

Anatomical context of Methoxytyramine

• In summary, our results indicate that dopamine in the substantia nigra is released from reserpine-sensitive storage sites and that pargyline-induced 3-methoxytyramine accumulation is a poor indicator of the local dopamine release [9].
• In vivo assessment of dopamine and norepinephrine release in rat neocortex: gas chromatography-mass spectrometry measurement of 3-methoxytyramine and normetanephrine [18].
• The principal metabolites of dopamine in fibroblast cells are 3-methoxytyramine 4-O-sulphate and 3-methoxytyramine [19].
• In naive mice, restraint stress increased 3-4-dihydroxyphenylacetic acid, homovanillic acid, and 3-methoxytyramine levels in the nucleus accumbens and 3-4-dihydroxyphenylacetic acid levels in the frontal cortex [20].
• Morphine was shown to enhance dopamine release in the rat olfactory tubercle, nucleus accumbens, prefrontal cortex and pyriform cortex, as assessed by increased 3-methoxytyramine (3-MT) levels and 3-MT accumulation after pargyline treatment [21].

Associations of Methoxytyramine with other chemical compounds

• Interstitial 3-methoxytyramine reflects striatal dopamine release: an in vivo microdialysis study [22].
• A new method with the sensitivity and specificity required to measure regional levels of 3-methoxytyramine (3-MT) and normetanephrine (NMN) in the rat cortex is described [18].
• Endogenous concentrations of DA, 3-methoxytyramine, 3,4-dihydroxyphenylacetic acid, and homovanillic acid were also measured in guinea pig and rat striatum following selective type A (clorgyline-treated) and type B (deprenyl-treated) MAO inhibition [23].
• Methylation (3-methoxytyramine) or absence of the 3-hydroxy group (tyramine) of dopamine resulted in total loss of activity [24].
• 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 [25].

Gene context of Methoxytyramine

• 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 [26].
• Stress-induced decrease of 3-methoxytyramine in the nucleus accumbens of the mouse is prevented by naltrexone pretreatment [27].
• In addition homovanillic acid (HVA) (or 3-methoxytyramine (3-MT) in pargyline-pretreated mice) (Peak 4) and somatostatin (Peak 5) were also measured in vivo [28].
• The affinity of ligands to BSA strengthened with progression of the metabolism in the order of DOPA less than dopamine less than 3-methoxytyramine less than homovanillic acid [29].
• Administered 1-C14-3,4-methylenedioxyphenethylamine led to the excretion of about 2% of the urinary C14 as conjugated dopamine and 3-methoxytyramine metabolites, in tranylcypromine treated rats [30].

Analytical, diagnostic and therapeutic context of Methoxytyramine

• A rapid and simple method for the determination of picogram levels of 3-methoxytyramine in brain tissue using liquid chromatography with electrochemical detection [2].
• Determination of 3-methoxytyramine in rat brain by HPLC with electrochemical detection and its correlation with dopamine function after administration of a monoamine oxidase inhibitor and L-3,4-dihydroxyphenylalanine [31].
• In addition to the above three metabolites, the level of 3-methoxytyramine, which is an indicator of the amount of DA released, greatly increased after treatment with a low dose (1 mg/kg) of clorgyline.(ABSTRACT TRUNCATED AT 250 WORDS)[32]
• Striatal 3-methoxytyramine as an index of dopamine release effects of electrical stimulation [33].
• Immobilization stress induced, in mice of both C57BL/6 (C57) and DBA/2 (DBA) strains, an increase in dihydroxyphenylacetic acid (DOPAC)/dopamine (DA) and homovanillic acid (HVA)/DA ratios and a reduction of 3-methoxytyramine (3-MT)/DA ratio in the caudatus putamen (CP) and nucleus accumbens septi (NAS) [34].

References