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PubMed1980

Highly sensitive method for the quantitation of homovanillic acid in cerebrospinal fluid.

Homovanillic acid in minute samples (50-100 microliters) of cerebrospinal fluid can be quantitated as its O-dimethylthiophosphinate methyl ester. The derivative is determined after glass capillary gas chromatography (GC) with high sensitivity by using a phosphorus-specific thermionic detector or by mass fragmentography, combined with a large sample volume split-splitless injector. The dimethylthiophosphinic esters show excellent stability against moisture and air. The precision of the overall procedure is 5.4% (GC) and 3.8% (GC-mass spectrometry). The method shows good linearity (r = 0.9999) over three orders of magnitude, from 500 pg to 500 ng. The lowest detectable concentration of homovanillic acid is 2-5 ng/ml. Concentrations of homovanillic acid determined in cerebrospinal fluid were 9.9-63.1 ng/ml (n = 10, mean = 30.9 ng/ml).

Dopamine↗

PubMed1981

Determination of dopamine, homovanillic acid and 3,4-dihydroxyphenylacetic acid in rat brain striatum by high-performance liquid chromatography with electrochemical detection.

Two procedures using liquid chromatography with electrochemical detection are described for the determination of dopamine (DA) and its two acidic metabolites, homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC), in subregions of rat striatum and nucleus accumbens. A strong cation-exchange column was used for DA analysis and a C18 reversed-phase column was used for the analysis of the metabolites. Effects of pH, temperature and percentage of methanol on the retention time of HVA and DOPAC were studied. Levels of these compounds in the subregions of rat stratum and nucleus accumbens are reported.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1971

Effect of folic acid by mouth on cerebrospinal fluid homovanillic acid and 5-hydroxyindoleacetic acid concentration.

Administration of 30 mg folic acid by mouth caused a significant fall in cerebrospinal fluid homovanillic acid concentration in 11 subjects. There was no significant change of 5-hydroxyindoleacetic acid concentration. The fall was less marked in five patients on anticonvulsant medication and failed to reach statistical significance. Neither homovanillic acid nor 5-hydroxyindoleacetic acid concentrations changed significantly when 15 mg folic acid was given in divided dosage for one, two, and four weeks. The effect appeared to be related to the height of serum-folate levels reached and to be independent of cerebrospinal fluid-folate levels, which did not change significantly. Possible mechanisms and their potential therapeutic application are discussed.

Administration, Oral↗

PubMed1993

Simultaneous analysis of homovanillic acid, 5-hydroxyindoleacetic acid, 3-methoxy-4-hydroxyphenylethylene glycol and vanilmandelic acid in plasma from alcoholics by high-performance liquid chromatography with electrochemical detection. Critical comparison of solid-phase and liquid-liquid extraction methods.

A method is described for the simultaneous determination of vanilmandelic acid, 3-methoxy-4-hydroxyphenylethylene glycol, 5-hydroxyindoleacetic acid, and homovanillic acid in a human plasma sample using reversed-phase high-performance liquid chromatography with column switching and amperometric detection. Two methods of sample preparation were tested. Liquid-liquid extraction yields better recoveries, is more selective and precise than solid-phase extraction and allows a shorter time of chromatographic analysis. Estimated plasma values of the metabolites from healthy controls are in good agreement with previously reported levels. Studies of alcoholics at the beginning of the delirium tremens provided different plasma levels of the metabolites, dependent on the different duration--and hence the severity--of the delirium.

Alcohol Withdrawal Delirium↗

PubMed1976

Effects of aminooxyacetic acid and baclofen on catalepsy, striatal homovanillic acid increase and antinociception caused by methadone in rats.

The effects of aminooxyacetic acid (AOAA) and baclofen on the catalepsy, striatal homovanillic acid (HVA) increase and antinociception caused by methadone were studied in rats. Antinociceptive responses were tested by the electric foot-shock method. A new type of stimulator unit which delivered nearly constant current over a wide range of output voltage and which was noiseless was designed and its construction is described. AOAA (25 mg/kg) which increases the cerebral concentration of gamma-aminobutyric acid (GABA) and baclofen (10 mg/kg), a structural analogue of GABA, did not change the catalepsy induced by methadone (5 mg/kg). AOAA (25 and 50 mg/kg) alone did not alter the striatal HVA content and had no effect on the methadone induced HVA increase. Baclofen (10 mg/kg) increased the striatal HVA content by 19% (P less than 0.01) and reduced the methadone-induced HVA increase by 36% (P less than 0.01). AOAA (25 mg/kg). These results suggest that narcotic analgesics might cause catalepsy and increase striatal dopamine turnover by some other mechanism than neuroleptics. The results support the suggestion that GABA might be involved in pain mechanisms.

Acetates↗

PubMed1993

Urinary excretion of homovanillic acid in workers exposed to manganese.

Homovanillic acid, an end product of dopamine catabolism, and manganese (Mn) were measured in the urine of 68 male workers exposed to Mn-containing dust in a dry alkaline battery plant or an Mn oxide and salt producing plant, and in 35 control male subjects. The geometric mean of the airborne concentration of inhalable (total) dust amounted to 0.95 and 1.37 mg/m3 in the dry alkaline battery plant and the Mn oxide and salt producing plant, respectively. In the latter, a higher prevalence of increased values of urinary homovanillic acid concentration was found. In the total population, there was a low but statistically significant positive correlation between the concentration of homovanillic acid and Mn in urine (r = 0.20, P = 0.04) but there was no significant correlation between the level of homovanillic acid in urine and Mn in airborne dust or duration of exposure. This observation might be compatible with the stimulation of dopamine turnover in the brain, which has been observed in the early phase of Mn intoxication in animals. However, the large variability in urinary homovanillic acid excretion in control subjects precludes the use of this biological indicator to detect early interference of Mn with the dopaminergic system.

Adult↗

PubMed1987

Disposition of homovanillic acid in the primate.

Prior studies have shown that homovanillic acid is the principal metabolite of dopamine in the primate central nervous system (CNS). In studies of primates given deuterated homovanillic acid systemically, however, only 50% of the administered amounts have been recovered in the urine over the next 4-48 hr. These findings have left it unclear whether there is a slowly turning-over compartment of homovanillic acid, conversion of homovanillic acid to another compound, or excretion of homovanillic acid from the body by a nonrenal route. We synthesized [3H]homovanillic acid and administered it intravenously to four rhesus monkeys. Over the subsequent 4 hr, 94.9 +/- 8.9% (SD) of the administered radioactivity was recovered in the urine, almost entirely as homovanillic acid. These results are consistent with the interpretation that, in primates, there is not a major body pool of homovanillic acid with slow turnover, nor is metabolism to other compounds significant, nor is there evidence for nonrenal excretion.

Animals↗

PubMed2004

Genetics of monoamine metabolites in baboons: overlapping sets of genes influence levels of 5-hydroxyindolacetic acid, 3-hydroxy-4-methoxyphenylglycol, and homovanillic acid.

BACKGROUND: Monoamine neurotransmitters (serotonin, dopamine, and norepinephrine) are associated with several psychiatric disorders. Limited evidence suggests that monoamine levels are heritable, but no information concerning genetic relationships among monoamines is available. Further genetic analysis can help explain phenotypic correlations among monoamine levels and might eventually help identify genes involved in response to therapy or risk of psychopathology. METHODS: Levels of the monoamine metabolites homovanillic acid (HVA), 5-hydroxyindolacetic acid (5-HIAA), and 3-hydroxy-4-methoxyphenylglycol (MHPG) were measured in cerebrospinal fluid from 271 baboons (Papio hamadryas). Variance components methods were used to estimate heritabilities, and multivariate analyses were used to estimate genetic correlations (pleiotropy) and environmental correlations between metabolites. RESULTS: Each metabolite exhibited significant heritability in baboons (5-HIAA: h(2) =.30 +/-.17; MHPG: h(2) =.36 +/-.16; HVA: h(2) =.50 +/-.19). Multivariate analyses revealed genetic correlations between 5-HIAA and HVA and between HVA and MHPG. Environmental correlations were found between 5-HIAA and HVA and between 5-HIAA and MHPG. CONCLUSIONS: Overlapping, nonidentical sets of genes influence individual variation in 5-HIAA, MHPG, and HVA levels among baboons. The phenotypic correlation between 5-HIAA and HVA observed in nonhuman primates and humans is likely due to both shared genetic and environmental factors. Genetic analyses of monoamine levels in primates can provide novel information concerning the genetics of variation among humans.

Analysis of Variance↗

PubMed1988

A central 6-hydroxydopamine lesion prevents fluphenazine-induced increase in plasma homovanillic acid.

Plasma and brain levels of the dopamine metabolite, homovanillic acid, were measured in rats after acute and chronic treatment with fluphenazine. After acute administration, homovanillic acid levels were increased in the whole frontal cortex, caudate nucleus, nucleus accumbens, anterior cingulate (supragenual) cortex, prefrontal cortex and plasma. Following chronic administration, the effects of single doses of fluphenazine in increasing homovanillic acid were markedly attenuated in the caudate nucleus, nucleus accumbens, the whole frontal cortex, anterior cigulate cortex and plasma, but not in the prefrontal (anteromedial) cortex. Following fluphenazine administration plasma homovanillic acid levels were correlated with homovanillic acid concentrations in whole frontal cortex (r = 0.63, p less than 0.01) and caudate nucleus (r = 0.51, p less than 0.05). Further, prior intracerebroventricular administration of 6-hydroxydopamine prevented the fluphenazine-induced increase in plasma homovanillic acid. These data suggest that in the rat, plasma and brain (caudate nucleus and whole frontal cortex) homovanillic acid levels change in a similar fashion during acute and chronic neuroleptic administration.

Animals↗

PubMed2000

Formation of homovanillic acid dimer by enzymatic or Fenton system - catalyzed oxidation.

Homovanillic acid is the most extensively employed reagent for the fluorometric detection of peroxidase. However, the assays based on the determination of the oxidation product of homovanillic acid do not allow a selective detection of the enzyme, because chemical or physical factors can interfere with the fluorometric determination. The aim of this work was to verify if other enzymatic or non-enzymatic systems might catalyze the homovanillic acid oxidation. The reaction was investigated by spectrophotometric and fluorometric assays; HPLC analysis was used to separate homovanillic acid from its oxidation product and to obtain information on the oxidation process. The results obtained showed that soybean lipoxygenase in the presence of hydrogen peroxide can oxidize homovanillic acid with the formation, by an o,o'-biphenyl linkage, of the corresponding dimer as the sole reaction product. The reaction followed Michaelis-Menten kinetics, for both homovanillic acid and hydrogen peroxide. Other systems, such as cytochrome c/H(2)O(2) and Fenton reagents, were also able to oxidize homovanillic acid to its dimer. It can be affirmed that possible interference by other oxidative systems - that could be present in the biological materials tested - should be considered in assays of peroxidase activity based on the detection of the dimer of homovanillic acid.

Catalysis↗

PubMed2007

Effect of strenuous exercise on urine concentrations of homovanillic acid, cortisol, and vanillylmandelic acid in sled dogs.

OBJECTIVE: To determine whether prolonged exercise by conditioned sled dogs affects urine concentrations of homovanillic acid (a metabolite of dopamine), vanillylmandelic acid (a metabolite of norepinephrine and epinephrine), and cortisol. ANIMALS: 24 conditioned Alaskan sled dogs (2 to 8.5 years old) that were in training for a multiday endurance race. PROCEDURES: Voided urine samples were collected from 4 groups of dogs (randomly selected from 54 dogs) after no exercise (control group; n = 6 dogs), completion of a 160km run (group A; 3), completion of a 420-km run (group B; 7), and completion of a 560-km run (group C; 6). Urine cortisol concentrations were determined by use of an immunoassay technique; urine vanillylmandelic acid and homovanillic acid concentrations were measured via high-performance liquid chromatography. RESULTS: Compared with the control group, urine cortisol concentration in groups A, B, and C was significantly different (5.33 x 10(4) +/- 2.62 x 10(4) microg/dL vs 1.04 x 10(4) +/- 2.31 x 10(5) microg/dL, 8.88 x 10(4) +/- 5.49 x 10(4) microg/dL, and 6.31 x 10(4) +/- 5.09 x 10(4) microg/dL, respectively). Urine homovanillic acid concentration did not differ among the 4 groups. Vanillylmandelic acid was not detected in any urine samples. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that prolonged exercise by sled dogs did not affect urine homovanillic acid concentration but did increase urinary cortisol secretion, which is indicative of adrenocortical stimulation. The apparent lack of vanillylmandelic acid in voided urine samples requires further investigation.

Animals↗

PubMed1982

The effects of amfonelic acid and some other central stimulants on mouse striatal tyramine, dopamine and homovanillic acid.

1 The concentrations of p- and m-tyramine, dopamine and homovanillic acid were measured in the mouse striatum following the subcutaneous administration of amfonelic acid, (+)-amphetamine or nomifensine.2 The administration of 2.5-25 mg/kg of amfonelic acid produced a reduction in p-tyramine that lasted at least 8 h. m-Tyramine was significantly increased and this was observed between 2 and 24 h after drug treatment. The levels of homovanillic acid were increased within 4 h after amfonelic acid administration.3 (+)-Amphetamine treatment (5 mg/kg) produced a reduction in p-tyramine observed up to 4 h after its administration and no significant changes in m-tyramine.4 The administration of 10 mg/kg of nomifensine produced no significant changes in p-tyramine, m-tyramine or homovanillic acid. By increasing the dose to 20 mg/kg, nomifensine produced an increase in p-tyramine and homovanillic acid.5 The present results support the view that amfonelic acid and (+)-amphetamine would respectively release granular or newly synthesized dopamine, both actions being accompanied by an increase in tyrosine hydroxylase activity and dopamine turnover which in turn reduces p-tyramine but produces no change or an increase in m-tyramine.6 The effects of nomifensine were observed after the administration of a relatively high dose (20 mg/kg), that was lethal to some mice (about 20%, at 2 h), and more likely to posses unspecific actions.

Amphetamine↗

PubMed1973

Failure of cerebrospinal fluid homovanillic acid to predict levodopa response in Parkinson's disease.

Lumbar cerebrospinal fluid homovanillic acid levels were estimated in 60 patients with Parkinsonism before and during levodopa treatment. There was a slight negative correlation between pretreatment CSF homovanillic acid levels and disability. There was no correlation between pretreatment homovanillic acid levels and clinical response to levodopa. Patients with high pretreatment levels did as well as those with depressed levels. High (normal or near normal) levels of CSF homovanillic acid in a patient with Parkinsonism do not necessarily indicate that the Parkinsonism will not respond to levodopa. These patients should receive the benefit of a trial of levodopa. There was also no correlation between homovanillic acid level during tratment and improvement. Patients with minimal increases in CSF homovanillic acid responded as well as those with greater elevations. Failure of levodopa to increase CSF homovanillic acid significantly does not indicate that the patient will not respond to levodopa and that levodopa should be discontinued. Other factors, such as vitamin B(6) consumption, should be investigated.

Dihydroxyphenylalanine↗

PubMedDate not supplied

Morning variations of plasma homovanillic acid in untreated schizophrenic patients.

Plasma concentrations of homovanillic acid were determined in samples obtained at 8.30 a.m. and 12.30 p.m. from 29 untreated schizophrenic patients, 14 males and 15 females. When the earlier samples were compared with the later, a significant decrease in mean plasma homovanillic acid level was observed, but only in the male patients. The morning fall was observed in 10 of 14 male patients and 6 of the 15 female patients. This morning rhythm in plasma homovanillic acid concentration may mask the putative rises in plasma homovanillic acid provoked by neuroleptic administration and may explain some of the observed differences between findings in studies involving the assessment of this metabolite.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1976

Gas chromatographic estimation of homovanillic acid in serum of normals and psychotic patients.

Homovanillic acid is extracted from 0.5 ml serum with ethyl acetate at acidic pH, and its pentafluoropropionic anhydride and hexafluoroisopropanol derivative injected into a 3% SE-30 column at 140 degrees C, fitted with an electron capture detector. In a group of normal volunteers (n = 42) a mean value of 62+/-45 mug/l was found. The distribution of the serum concentrations was found to be bimodal. Using the same procedure for the homovanillic acid estimation in cerebrospinal fluid (CSF), mean values of 73.0+/-41 mug/l serum and 68+/-36 mug/l CSF were found for a group of 22 untreated patients with paranoid-hallucinatory syndrome. After treatment with neuroleptics, for 1 week to 1 month, the homovanillic acid concentration increased significantly only in the CSF. By the procedure described, other acidic metabolites of biogenic amines are extracted together with homovanillic acid and can also be estimated in the same sample.

Chromatography, Gas↗

PubMed1991

Effects of neuroleptic treatment on symptoms of schizophrenia and plasma homovanillic acid concentrations.

Measurement of plasma concentrations of the dopamine metabolite, homovanillic acid, is an indirect tool to assess changes in dopamine turnover in schizophrenic patients. Plasma homovanillic acid concentrations have been reported to decrease during neuroleptic treatment, with the decrement correlating with symptomatic improvement in symptoms of schizophrenia. The present study tested the hypothesis that neuroleptic drugs decrease plasma homovanillic acid concentrations in those schizophrenic patients who improve with administration of neuroleptic drugs but not in patients who fail to display a treatment response. Twenty schizophrenic men who remained drug free for at least 2 weeks were treated with 20 mg/d of haloperidol for 5 weeks. Symptoms and plasma homovanillic acid concentrations were assessed on the last drug-free day and weekly for 5 weeks. Mean plasma homovanillic acid concentrations decreased in the group of patients who responded to neuroleptic treatment and did not change in the group of patients who did not improve. These findings suggest that there may be a qualitative distinction between responders and nonresponders to dopamine antagonists.

Administration, Oral↗

PubMed1976

Homovanillic acid transport by the spinal cord.

Spinal subarachnoid perfusions of rhesus monkeys were performed to study spinal transport of homovanillic acid in control and probenecid-treated animals. Homovanillic acid enters capillaries within spinal tissue throughout the spinal cord. The mean capillary exchange half-time for homovanillic acid was 19.2+/-2.8 minutes; probenecid did not affect this value significantly. Despite its polar nature, homovanillic acid crosses cell boundaries easily and equilibrates in a distribution volume (55 percent) approaching the total water space. The spinal cord clears homovanillic acid from 21+/-4 mul per minute of cerebrospinal fluid. The rate of clearance after probenecid administration was not significantly different. The apparent diffusion coefficient in tissue of homovanillic acid approximated the diffusion coefficient in water (8.0 X 10(-6) cm2 per second). The data show that homovanillic acid is transported by capillaries throughout spinal tissue by a mechanism largely insensitive to inhibition by probenecid. Lumbar cerebrospinal fluid concentrations of homovanillic acid even after probenecid administration therefore reflect only part of the total dopamine metabolism.

Animals↗

PubMed1991

Diazepam and haloperidol. Effect on regional brain homovanillic acid levels.

Diazepam lowered homovanillic acid levels in brain regions from untreated and haloperidol-treated rats. However, there was evidence of a biphasic effect in that 2 mg/kg was more effective than 10 mg/kg under several conditions. Diazepam was more effective in restoring regional HVA toward control levels following doses of haloperidol in the low clinical range (0.1 to 0.2 mg/kg) than following higher doses. With respect to maximizing dopamine receptor blockade and minimizing compensatory presynaptic activity in the acute treatment of psychotic conditions, our data provide some support for the use of modest doses of neuroleptics and benzodiazepines.

Adult↗