Urine catecholamines

The maximum level of HMMA in the urine occurred 72 hours after exposure, which coincides with the time period for maximum urine catecholamine levels. There was a direct relationship between blood cholinesterase inhibition and catecholamine (adrenaline and noradrenaline) levels in the urine and blood (Brzezinski and Ludwicki 1973). Maximum inhibition of cholinesterase activity and maximum plasma catecholamine occurred during the first I-2 hours after exposure. However, catecholamine levels returned to normal more rapidly than cholinesterase activity. It was proposed that high levels of acetylcholine, which are normally associated with cholinesterase activity inhibition, caused a release of catecholamines from the stores in the adrenals. 

Urine catecholamines may also serve as biomarkers of disulfoton exposure. No human data are available to support this, but limited animal data provide some evidence of this. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in female rats, respectively, within 72 hours of exposure (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). Because organophosphates other than disulfoton can cause an accumulation of acetylcholine at nerve synapses, these chemical compounds may also cause a release of catecholamines from the adrenals and the nervous system. In addition, increased blood and urine catecholamines can be associated with overstimulation of the adrenal medulla and/or the sympathetic neurons by excitement/stress or sympathomimetic drugs, and other chemical compounds such as reserpine, carbon tetrachloride, carbon disulfide, DDT, and monoamine oxidase inhibitors (MAO) inhibitors (Brzezinski 1969). For these reasons, a change in catecholamine levels is not a specific indicator of disulfoton exposure. 

Pritchard J, Barnes J, Germond S, Hartman O, deKraker J, Lewis I, et al. Stage and urine catecholamine metabolite excretion in neuroblastoma. Lancet 1989 1 514-5. 

Lehmann, M., Dorges, V., Huber, G., ZoUner, G., Spori, U., Keul, J. (1983). ZumVeihalten der fieienKalecholamine im Blut und Ham bei Sanitatem und arzten wahrend des Einsatzes [Behavior of flee plasma and urine catecholamines of ambulance men and physicians during medical service]. International Archives of... 

Disulfoton exposure altered catecholamine levels in animals, and this hormonal imbalance may be associated with elevated acetylcholine levels (Brzezinski 1969, 1972, 1973 Brzezinski and Ludwicki 1973 Brzezinski and Rusiecki 1970 Wysocka-Paruszewska 1970, 1971). In these studies, acute dosing with disulfoton caused increases in urinary and plasma noradrenaline and adrenaline levels, accompanied by decreases of adrenaline in the adrenal glands, in rats. In addition, the major urinary metabolite of catecholamine metabolism, 4-hydroxy-3-methoxymandelic acid (HMMA), was recovered in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1970,... 

Elevated catecholamine concentrations in the urine were also observed in rats dosed with 0.625 mg/kg/day of disulfoton every other day for 76 days (Brzezinski and Rusiecki 1970). Urinary catecholamine levels plateaued between 16 and 36 days, followed by a gradual decline for the next 40 days. However, these levels were still elevated at day 76. 

Increased levels of urinary catecholamines may also be associated with accumulation of acetylcholine that resulted from acetylcholinesterase inhibition by disulfoton. No human data were located to support this, but limited animal data provide some evidence. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in rats, respectively, within 72 hours (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). 

Brzezinski J. 1969. Catecholamines in urine of rats intoxicated with phosphororganic insecticides. Dissertationes Pharmaceuticae et Pharmacologicae 21 381-385. 

Brzezinski J, Ludwicki K. 1973. The interrelationship of the changes of acetylcholine esterase and catecholamines blood and urine levels in rats poisoned with Disyston. Pol J Pharmacol Pharm 25 313-316. 

Brzezinski J, Rusiecki W. 1970. The excretion of catecholamines in rat urine related to Disyston poisoning. Dissertationes Pharmaceuticae et Pharmacologicae 22 507-511. 

Figure 4.10 Direct analysis of catecholamines in urine sample. Column, Asahipak ES-502C eluent, 75 mM succinic acid + 25 mM borate buffer (pH 6.10) containing 0.5 mM EDTA flow rate, 1.0 min-1 detection, fluorescence reaction detection Ex. 350 nm. Peaks-. 1, adrenaline-, 2, noradrenaline-, and 3, dopamine.

Chan EC, Ho PC. 2000. High-performance liquid chromatog-raphy/atmospheric pressure chemical ionization mass spec-trometric method for the analysis of catecholamines and metanephrines in human urine. Rapid Commun Mass Spectrom 14 1959. 

Peterson ZD, Collins DC, BowerbankCR, Lee ML, Graves SW. 2002. Determination of catecholamines and metanephrines in urine by capillary electrophoresis-electrospray ioniza-tion-time-of-flight mass spectrometry. J Chromatogr B Analyt Technol Biomed Life Sci 776 221. 

Other components of the urine are conjugates with sulfuric acid, glucuronic acid, glycine, and other polar compounds that are synthesized in the liver by biotransformation (see p. 316). In addition, metabolites of many hormones (catecholamines, steroids, serotonin) also appear in the urine and can provide information about hormone production. The proteohormone chorionic gonadotropin (hCG, mass ca. 36 kDa), which is formed at the onset of pregnancy, appears in the urine due to its relatively small size. Evidence of hCG in the urine provides the basis for an immunological pregnancy test. 

There are stability problems in urines stored for analysis. Fifty percent of delta-aminolevulinic acid was lost in specimens stored without preservative and exposed to light for 24 hours (V3). The loss increased to 80% in 48 hours, 85% in 72 hours, and 95% in 2 weeks. However, the same specimens acidified with tartaric acid and stored in the dark lost 2% of the aminolevulinic acid in 72 hours and 6% in 2 weeks (V3). The destruction of catecholamines collected in nonacidified urine specimens is well documented (Cll). Urinary acid phosphatase was destroyed on freezing (S15). The effect was related to increasing salt concentration during freezing and was prevented by the addition of albumin (S15). 

An important area of direct biochemical interference is that caused by fluorescent or fluorescent quenching materials in the blood or urine after the administration of a drug. These interferences may be observed during catecholamine analysis in urine from patients receiving -methyldopa, tetracyclines, chlortetracyclines, oxytetracycline, erythromycin, chlorpro-mazine, or quinidine (A2, G5). 

Cll. Crout, J. E., Catecholamines in urine. Stand. Methods Clin. Chem. 3, 62-80 (1967). 

Drug/Lab test interactions Methyidopa may interfere with tests for Urinary uric acid by phosphotungstate method serum creatinine by alkaline picrate method AST by colorimetric methods. Because methyidopa causes fluorescence in urine samples at the same wavelengths as catecholamines, falsely high levels of urinary catecholamines may occur and will interfere with the diagnosis of pheochromocytoma. 

Changes in catecholamines and 3-O-methyl metabolite concentrations in human plasma Erythropoietin in pharmaceutical products 3,4-methylenedioxymethamphetamine, 3,4-methylenedioxyamphetamine, amphetamine, and methamphetamine in rat urine Azoxystrobin, kresoxim-methyl, and trifloxystrobin fungiddes ... 

Brandsteterova E, Kubalec P, Skacani 1, Balazovjech 1. HPLC-Ed determination of catecholamines and their metabolites in urine. Neoplasma 41, 205-211, 1994. 

Assay of catecholamines in urine by ion exchange chromatography with electrochemical detection... 

The initial report of sustained, lower urinary cortisol levels in PTSD highlighted the disassociation between cortisol and catecholamine levels in PTSD. Norepinephrine and epinephrine levels assayed from the same urine specimens revealed elevations in both of these catecholamines, while cortisol levels in PTSD fell within the normal range of 20-90 pg/day, indicating that the alteration was not in the hypoadrenal or endocrinopathologic range (Mason et al. 1986). This finding established the expectation that alterations in basal levels of cortisol might be subtle, and not easily differentiated from normal values (Mason et al. 1986). 

The presence of a-methyldopa and its metabolites in the urine reduces the diagnostic value of urinary catecholamine measurements as an indicator of pheochro-mocytoma, since these substances interfere with the fluorescence assay for catecholamines. 

Norepinephrine and epinephrine can be metabolized by several enzymes, as shown in Figure 6-6. Because of the high activity of monoamine oxidase in the mitochondria of the nerve terminal, there is significant turnover of norepinephrine even in the resting terminal. Since the metabolic products are excreted in the urine, an estimate of catecholamine turnover can be obtained from laboratory analysis of total metabolites (sometimes... 

Dichloromethane (> 6.3 mmol/kg bw) administered to rats by gavage induced increased urinary excretion of catecholamines in the urine in rats cytomorphological changes and a decrease in chromafim reaction were observed in the adrenal medulla at a dose level of 15.6 mmol/kg bw (1330 mg/kg) (Marzotko Pankow, 1987). 

Degradation of catecholamines The catecholamines are inacti vated by oxidative deamination catalyzed by monoamine oxidase (MAO), and by O-methylation carried out by catechol-O-methyl-transferase (COMT, Figure 21.15). The two reactions can occur in either order. The aldehyde products of the MAO reaction are axi dized to the corresponding acids. The metabolic products of these reactions are excreted in the urine as vanillylmandelic acid, metanephrine, and normetanephrine. 

URINE EXTRACTION. Neonatal urine (15 cm3 if the 24-hr volume was greater than 100 cm3 or 10 cm3 if less), normal adult urine (10 cm3), or urine of patients with suspected catecholamine secreting... 

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