Levels Of Phenylacetic Acid Research Articles

Phenylethylamine metabolism in Tourette's syndrome

Beta-phenylethylamine, phenylalanine, and phenylacetic acid were examined in 24-hour urine samples and/or plasma samples obtained from 28 medication-free patients with Tourette's syndrome and 20 control subjects matched for age and education. Statistical analyses revealed that Tourette patients had lower plasma phenylalanine and urinary free beta-phenylethylamine compared with the controls, but did not differ on urinary total levels of phenylacetic acid. Fifty percent of the Tourette patients had a urinary beta-phenylethylamine level that was lower than the lowest control subject. In addition, urinary beta-phenylethylamine levels were inversely related to several scores from the Tourette Syndrome Global Scale. These data suggest that abnormalities in synthesis or metabolism of beta-phenylethylamine may be involved in the etiology of some patients with Tourette's syndrome.

Septic encephalopathy. Evidence for altered phenylalanine metabolism and comparison with hepatic encephalopathy

We elected to test the hypothesis that the metabolic encephalopathy associated with systemic sepsis may have a pathogenesis that is similar to hepatic encepathology, ie, as the consequence of hepatic dysfunction that induces alterations in synthesis of catecholic and noncatecholic neurotransmitters. Eleven patients with septic encephalopathy were compared with nine patients with septic encephalopathy and nine normal controls with respect to blood and cerebrospinal fluid (CSF) amino acid profile, phenylethylamine and its metabolite phenylacetic acid, and blood ammonia. Blood and CSF levels of phenylacetic acid increased markedly in septic and hepatic encephalopathy while CSF phenylethylamine levels were not increased in either condition, presumably due to rapid turnover. The CSF concentrations of all the aromatic amino acids were increased in hepatic encephalopathy, whereas in the patients with sepsis, only phenylalanine levels were increased. Evidence of stimulated neutral amino acid transport into brain was demonstrated in hepatic not septic encephalopathy and appeared to correlate with the CSF glutamine concentration. Blood ammonia levels were increased in hepatic but not in septic encephalopathy. Our data support the hypothesis that metabolites of phenylethylamine contribute to encephalopathy in systemic sepsis and hepatic failure; however, the entities differ in other respects.

Urinary phenylacetic acid excretion in depressive patients.

Phenylacetic acid (PAA), a metabolite of phenylethylamine, has been found in the urine of depressed patients at lower levels than in control subjects. It has been suggested that the determination of PAA in urine could be used as a biological marker of the depressive condition. In this study the levels of PAA in urine were investigated by gas-liquid chromatography in 39 patients diagnosed as having major depression according to DSM-III criteria, and in 32 healthy subjects. The values found in the patients were markedly lower than in controls. No relationship was found between the decrease of PAA excretion and weight loss. Using a discriminant equation, a value of 69% was obtained for both sensitivity and specificity. The results suggest that the determination of urine PAA could be a biological parameter comparable to the dexamethasone suppression test.

Determination of phenylacetic acid in cerebrospinal fluid by gas chromatography-mass spectrometry.

Using gas chromatography-mass spectrometry, we developed a sensitive and reliable technique to measure phenylacetic acid (PAA), an oxidatively deaminated metabolite of beta-phenylethylamine (PEA), in small amounts of cerebrospinal fluid (CSF). In a preliminary analysis, PAA concentrations in depressive patients were significantly lower than those in controls, while there were no differences in PAA levels between schizophrenic patients and controls. This suggests a possible link between the decreased PEA metabolism in the brain and the etiology of depression. However, further studies are needed to clarify the effects of neuroleptics and antidepressants on PAA levels in CSF, since the samples were obtained without regard to medication in the present study. In control subjects, a U-shaped distribution was obtained when the values of PAA were plotted as a function of age. There were no sex differences and no significant concentration gradients in CSF PAA levels.

Growth Regulators in Developing Effective Root Nodules of the Garden Pea (Pisum sativum L.)

Summary Levels of auxins and abscisic acid (ABA) in developing pea root nodules and uninfected roots of the garden pea ( Pisum sativum L.) were determined by gas liquid chromatography of methanol extracts. Higher levels of ABA and two auxins, indole-3-acetic acid (IAA) and indole-3-propionic acid (IPA), were detected in root nodules than in uninfected roots. In roots higher levels of ABA and phenylacetic acid (PAA) were found in the terminal 5 mm segment which included the root apical meristem but the reverse was true for IPA. Between the 2nd and 5th weeks of development the levels of IAA and PAA in nodules decreased. ABA and IPA concentratations appear to increase at the onset of nodule senescence. Higher levels of ABA were associated with the nodule meristem than with the pink-colored region of infected cells, the site of symbiotic nitrogen fixation.

Alterations in trace amine and trace acid concentrations in isolated aggressive mice.

We have used an animal model of aggression, the isolation syndrome in mice, to examine the possible role of the trace amines, beta-phenylethylamine (PEA), meta-tyramine (m-TA) and para-tyramine (p-TA) in aggressive behaviour. The brain, plasma and urinary levels of PEA, m-TA and p-TA, and their respective major acid metabolites, phenylacetic acid (PAA), meta-hydroxyphenylacetic acid (m-HPA) and para-hydroxyphenylacetic acid (p-HPA) were measured in isolated aggressive mice (after fighting), and in group housed controls. The urinary levels of PEA, m-TA, PAA, m-HPA and p-HPA, and the plasma levels of PAA and p-HPA were significantly lower in isolated aggressive mice. Similarly, the whole brain levels of PEA, p-TA, PAA and p-HPA tended to be reduced. In contrast, the brain levels of m-TA and m-HPA tended to increase. It should be noted, however, that the present procedure did not dissociate the stress and aggression components of the isolation syndrome, and, therefore, further experiments are required to determine whether the observed neurochemical changes are functionally related to increased aggression.

Plasma levels of phenylacetic acid, m- and p-hydroxyphenylacetic acid, and platelet monoamine oxidase activity in schizophrenic and other patients

Blood from chronic schizophrenic patients in two hospitals (A and B) and from institutional and noninstitutional controls was analyzed for platelet monoamine oxidase (MAO) activity toward three different substrates (tryptamine, phenylethylamine, and p-tyramine) and for plasma levels of conjugated and unconjugated phenylacetic acid (PAA) and m- and p-hydroxyphenylacetic acids (mHPA and pHPA). Compared to the controls, schizophrenic patients were found to have significantly reduced MAO activity. Although significant differences were found between unconjugated PAA (reduced) in Hospital B, conjugated pHPA (increased) in Hospital A, and conjugated PAA (increased) in Hospitals A and B and noninstitutional controls, the most consistent significant finding was a reduced unconjugated mHPA in both groups of schizophrenic patients compared with both control groups.

Longitudinal urinary excretion of some “trace” acids in a human male

Conjugated and unconjugated urinary levels of phenylacetic acid (PAA), m-hydroxyphenylacetic acid ( m-HPA) and p-hydroxyphenylacetic acid have been determined for 24-h urine samples obtained from a single healthy male over a 28-day period. Gas chromatographic—electron-capture and mass spectrometric—integrated ion current techniques incorporating appropriate internal standards were used. The average urinary excretion values obtained were (in mg/24 h): PAA unconjugated 0.67, conjugated 96.6; m-HPA unconjugated 7.3, conjugated < 0.1; p-HPA unconjugated 22.4, conjugated < 1.2. Following the ingestion of appropriate deuterated amino acid precursors the expected urinary deuterated trace acids were identified and quantitated; in the case of deuterated phenylethylamine, m-HPA and p-HPA as well as PAA were identified and quantitated. This is the first evidence of phenylethylamine hydroxylation in the human. The longitudinal excretion of the trace acids was compared with that of the trace amines.

Changes in endogenous levels of IAA and PAA in rice seed during development, prediction of auxin signaling proteins and docking for its binding efficiency with auxin molecules

Indole-3-acetic acid (IAA) and phenyl acetic acid (PAA) are two major physiologically active auxins, found in higher plants. The objective of this study was to evaluate changes in the endogenous levels of IAA and PAA in rice (Oryza sativa) seed and predict probable transporter and efflux (signaling) proteins for docking with auxins from the available rice genome data. IAA and PAA were estimated during rice seed development using sensitive and specific antibodies against each hormone. The levels of IAA and PAA were higher when sink size development was at its peak, suggesting an important role played by the auxin in sink size development of rice seed. Furthermore, auxin binding transporters proteins of rice were confirmed for docking purpose and compared with Arabidopsis and maize proteins. In this context, PAA docked with known IAA proteins; although, docking score of IAA was higher than that of PAA in rice seed. Twelve genes of the auxin efflux carrier (PIN family) of rice were also analysed for phylogeny relatedness with Arabidopsis and maize, to further understanding auxin concentrations and efflux within rice seeds. The predicted PIN proteins for IAA efflux of rice showed docking affinities with PAA, revealed its role in maintaining physiological concentrations of auxins in rice seeds.

Multiple biochemical correlates of manic-depressive illness

Davis Bruce A. and Alan A. Boulton: The Trace Amines and Their Acidic Metabolites in Depression — An Overview Progr. Neuro-Psychopharmacol. & Biol. Psychiat. 1994, 18(1): 17–45.1.1. Investigations of the role of the trace amines (phenylethylamine, tryptamine, m- and p-tyramine) and their acidic metabolites (phenylacetic, indoleacetic, m- and p-hydroxyphenylacetic acids) in depression are reviewed.2.2. The evidence for the phenylethylamine hypothesis of depression is mixed.3.3. Reduced phenylacetic acid levels in urine, plasma and CSF and changes in those levels during treatment with antidepressants show potential as state markers for depression.4.4. Impaired p-tyramine conjugation following a tyramine challenge may be a good trait marker for depression.