5-Hydroxyindolacetic acid

The problem of selectivity is the most serious drawback to in vivo electrochemical analysis. Many compounds of neurochemical interest oxidize at very similar potentials. While this problem can be overcome somewhat by use of differential waveforms (see Sect. 3.2), many important compounds cannot be resolvai voltammetrically. It is generally not possible to distinguish between dopamine and its metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) or l tween 5-hydroxytryptamine (5-HT) and 5-hydroxyindolacetic acid (5-HIAA). Of even more serious concern, ascorbic acid oxidizes at the same potential as dopamine and uric acid oxidizes at the same potential as 5-HT, both of these interferences are present in millimolar concentrations... 

One important mechanism of serotonin elimination is the (re-) uptake, e.g. by platelets. Furthermore, serotonin is metabolized by monoaminox-idase to 5-hydroxyindoleacetaldehyde and, subsequently, by an aldehyde dehydrogenase to 5-hydroxyindolacetic acid. The vascular effects of serotonin are complex. The direct interaction with vascular smooth muscle induces a vasoconstriction, whereas the stimulation of 5-HT-receptors on the endothelium induces the release of vasorelaxant factors with a dilatation as a result. An intravenous application of serotonin increases the pressure in the pulmonary circulation. A continuous infusion results... 

FIGURE 18.1 Comparison of cerebrospiral fluid (CSF) concentrations of neuropeptide and monoamine metabolites in people who were 111 (underweight) and in those with long-term recovery from anorexia nervosa (AN). The CSF values in AN compared to healthy control women, where control mean values are set to 0. CRH, corticotropin-releasing hormone HVA, homovamillie acid NPY, neuropeptide Y REC, recovered SHIAA, 5-hydroxyindolacetic acid. 

TCDD was investigated. No changes were found in epinephrine and dopamine in the hypothalamus or in dopamine and its metabolites in the striatum. However, tryptophan (a precursor of serotonin) levels in plasma and brain were increased and this was paralleled by increases in brain serotonin and 5-hydroxyindolacetic acid (the major serotonin metabolite) (Rozman et al. 1991). Based on the results of these experiments, Rozman et al. (1991) proposed that decreased PEPCK activity decreases gluconeogenesis and leads to increased plasma concentrations of glycogenic amino acids, such as tryptophan. Increased tryptophan leads to increase in serotonin release in the brain and to appetite... 

Indoleamines in urine. 5-Hydroxyindolacetic acid (5-HIAA) is the principle metabolite of the neurotransmitter 5-HT and is excreted in urine. It is naturally fluorescent (excitation 280 nm and emission 360 nm, using a xenon lamp). The selectivity of fluorescence detection means that a very simple and rapid assay is possible. Provided the pH of the eluent is controlled in the region 5.1-5.4 (the exact value depends upon the make of Cl8 columns being used) 5-HIAA can be resolved from the front and... 

Paez X, Hernandez L. Simultaneous brain and blood microdialysis study with a new removable venous probe. Serotonin and 5-hydroxyindolacetic acid changes after D-norfenfluramine or fluoxetine. Life Sci 1996 58(15) 1209-1221. 

Deoxynivalenol, also known as DON or vomitoxin, is a trichothecene mycotoxin that affects brain neurochemistry (e.g., dopamine and 5-hydroxyindolacetic acid), leading to nausea and appetite suppression. Feed refusal or decreased feed intake occurs through a learned response known as "taste aversion."... 

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