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PubMed1991

Thioether excretion in urine of applicators exposed to 1,3-dichloropropene: a comparison with urinary mercapturic acid excretion.

The excretion of thioethers in urine of applicators occupationally exposed to the soil fumigant 1,3-dichloropropene (DCP) was determined by the thioether assay. The mercapturic acid metabolite of E-1,3-dichloropropene, N-acetyl-S-(E-3-chloropropenyl-2-)-L-cysteine (E-DCP-MA), was the reference compound in the thioether assay. The mean recovery of E-DCP-MA was 58.5% (coefficient of variation (CV) 9%, n = 4). In non-exposed men mean background of urinary thioethers was 6.05 mmol SH/mol creatinine (n = 56). In applicators exposed to soil fumigants containing DCP, urinary excretion of thioethers followed first order elimination kinetics. Urinary half lives of elimination of thioethers were 8.0 (SD 2.5) hours based on excretion rates and 9.5 (SD 3.1) hours based on creatinine excretion. The urinary half life of elimination of thioethers was almost twofold higher compared with half lives of elimination of the mercapturic acids of Z- and E-1,3-dichloropropene. The post- minus pre-shift thioether concentrations in urine and the cumulative urinary thioether excretions correlated well with exposure to DCP. In urine samples the mean thioether concentration was 1.38 higher than mean DCP mercapturic acid concentration. This suggests the presence of unidentified thioether metabolite(s) due to exposure to soil fumigants containing DCP. According to the present data, an eight hour time weighted average exposure to the Dutch occupational exposure limit of 5 mg/m(3) DCP results in a post- minus pre-shift thioether concentration of 9.6 mmol SH/mol creatinine (95% confidence interval (95%CI) 7.4-11.8 mmol SH/mon creatinine) and in a cumulative thioether excretion of 139 micromol SH (95% CI 120-157 micromol SH). It is concluded that the thioether assay can be used to assess comparatively high levels of exposure to DCP.

Acetylcysteine↗
PubMedDate not supplied

Furosemide compounds enhance urinary excretion of active kallikrein independently of their effects on urinary electrolyte excretion.

The chemical and diuretic effects of furosemide on the excretion and activation of urinary prokallikrein were investigated in rats by treatment with furosemide compounds with a range of diuretic activity or amiloride hydrochloride or the vehicle. Diuresis occurred with furosemide and benzyl furosemide, but not with isofurosemide, amiloride hydrochloride, or the vehicle. The urinary excretion rate of active kallikrein was significantly elevated above controls throughout the 72 h of treatment with all of the drugs tested, regardless of the level of diuresis or the rate of urinary electrolyte excretion. In contrast, the urinary excretion rate of total kallikrein (prokallikrein + active kallikrein) was unchanged in all groups. These data indicate that furosemide derivatives increase the activation, but not the excretion, of urinary prokallikrein and that these effects are unrelated to the chemical structure or diuretic activity of the compounds or to overall changes in urinary electrolyte excretion rates.

Animals↗
PubMed1995

Biliary cefpiramide excretion: its relation to biliary excretion of bile acids and sulfobromophthalein.

Cefpiramide, a beta-lactam antibiotic, has been reported to be excreted from hepatocytes into the bile by a carrier-mediated system. Herein, the relationship of biliary cefpiramide excretion to the excretion of bile acids and sulfobromophthalein was studied in rats. Biliary cefpiramide excretion was markedly inhibited by sulfobromophthalein, lithocholate-3-O-glucuronide and taurolithocholate-3-sulfate, whereas it was not inhibited by ursodeoxycholate or taurocholate. However, the inhibitory effect of cefpiramide on the biliary excretion of sulfobromophthalein or lithocholate-3-sulfate was very small. These findings indicate that, although cefpiramide is excreted by a process common to organic anions and bile acid sulfate and glucuronide, two or more excretory pathways for organic anions exist and cefpiramide has affinity for only one of these carriers.

Animals↗
PubMed1989

Effects of propylthiouracil on the biliary clearance of thyroxine (T4) in rats: decreased excretion of 3,5,3'-triiodothyronine glucuronide and increased excretion of 3,3',5'-triiodothyronine glucuronide and T4 sulfate.

The liver metabolizes T4 by deiodination and conjugation to T4 glucuronide (T4G), but little information exists about the formation of T4 sulfate (T4S) in vivo. We have examined the excretion of T4G, T4S, T3 and rT3 glucuronide (T3G and rT3G) in bile, collected under pentobarbital anesthesia 0-8 h or 17-18 h after iv [125I]T4 injection to control and 6-propyl-2-thiouracil (PTU)-treated rats. Radioactivity in bile, plasma, feces, and urine was analyzed by Sephadex LH-20 chromatography and HPLC. PTU induced a 2-fold increase in the biliary excretion of total radioactivity (26.6% vs. 15.0% dose between 0-8 h; 2.0% vs. 1.0% dose between 17-18 h). Biliary metabolites, 17-18 h after T4 injection, in control vs. PTU rats amounted to (percent dose): T4G, 0.44 vs. 0.75; T3G, 0.19 vs. 0.07; rT3G, 0.02 vs. 0.15; and T4S, 0.06 vs. 0.32. Similar results were obtained for control rats when bile was collected between 7-8 h after iv T4. The excretion rate of T3G was lower and that of rT3G higher when bile was continuously collected for 8 h immediately after T4 administration, probably due to prolonged experimental stress. However, regardless of the period of bile collection, PTU induced a more than 24-fold decrease in the T3G/rT3G ratio and a 5-fold increase in T4S excretion. In the animals killed 18 h after T4 injection, PTU treatment increased plasma T4 retention by 50%, reduced urinary I- excretion by 74%, and increased fecal radioactivity by 47%. No conjugates were detected in feces, and the distribution of fecal T4:T3:rT3 was 70:18:2 in control and 68:7:6 in PTU-treated rats. The results indicate that 1) the glucuronidative clearance of T4 is not affected by PTU; 2) the T3G/rT3G ratio in bile is a sensitive indicator of type I deiodinase inhibition; 3) T4 undergoes significant sulfation in rats in vivo, and 4) biliary excretion of T4S is enhanced if its type I deiodination is inhibited.

Animals↗
PubMed1977

Catecholamine excretion in "idiopathic" edema: decreased dopamine excretion, a pathogenic factor?

In 16 women with idiopathic edema, urinary dopamine excretion was decreased when compared to control women (146 +/- 13 SE ng/ml/m2 vs. 212 +/- 32, P less than 0.05 in the supine position and 140 +/- 9 vs. 199 +/- 20, P less than 0.005 combined values of supine and recumbent positions) and was also lower when pooled values for urinary dopamine excretions both before and after furosemide were compared in idiopathic edema patients and in control subjects (270 +/- 30 ng/ml vs. 480 +/- 70, P less than 0.05). These patients have lower basal sodium excretions, decreased tubular rejection fractions of sodium in the upright position and lower urinary sodium excretions following furosemide administration. The urinary sodium and dopamine excretions before and following furosemide are positively correlated in control (P less than 0.05), idiopathic edema patients (P less than 0.02) and in both groups combined (P less than 0.005). Idiopathic edema patients have normal urinary noradrenaline and adrenaline excretions but, as previously observed, elevated: 1) plasma renin activity while either recumbent or upright, and 2) plasma aldosterone concentrations while upright. These results suggest that a decrease in urinary dopamine, a catecholamine recently recognized to have natriuretic action, possibly reflects a suppression of the renal dopaminergic system and may contribute to the excessive sodium retention in idiopathic edema either directly or indirectly through the renin-aldosterone system.

Adult↗
PubMed2004

The giant mudskipper Periophthalmodon schlosseri facilitates active NH(4)(+) excretion by increasing acid excretion and decreasing NH(3) permeability in the skin.

Periophthalmodon schlosseri is an amphibious and obligatory air-breathing teleost, which is extremely tolerant to environmental ammonia. It actively excretes NH(4)(+) in ammonia loading conditions. For such a mechanism to operate efficaciously the fish must be able to prevent back flux of NH(3). P. schlosseri could lower the pH of 50 volumes (w/v) of 50% seawater in an artificial burrow from pH 8.2 to pH 7.4 in 1 day, and established an ambient ammonia concentration of 10 mmol l(-1) in 8 days. It could alter the rate of titratable acid efflux in response to ambient pH. The rate of net acid efflux (H(+) excretion) in P. schlosseri was pH-dependent, increasing in the order pH 6.0<7.0<8.0<8.5. Net acid flux in neutral or alkaline pH conditions was partially inhibited by bafilomycin, indicating the possible involvement of a V-type H(+)-ATPase. P. schlosseri could also increase the rate of H(+) excretion in response to the presence of ammonia in a neutral (pH 7.0) external medium. Increased H(+) excretion in P. schlosseri occurred in the head region where active excretion of NH(4)(+) took place. This would result in high concentrations of H(+) in the boundary water layer and prevent the dissociation of NH(4)(+), thus preventing a back flux of NH(3) through the branchial epithelia. P. schlosseri probably developed such an 'environmental ammonia detoxification' capability because of its unique behavior of burrow building in the mudflats and living therein in a limited volume of water. In addition, the skin of P. schlosseri had low permeability to NH(3). Using an Ussing-type apparatus with 10 mmol l(-1) NH(4)Cl and a 1 unit pH gradient (pH 8.0 to 7.0), the skin supported only a very small flux of NH(3) (0.0095 micromol cm(-2) min(-1)). Cholesterol content (4.5 micromol g(-1)) in the skin was high, which suggests low membrane fluidity. Phosphatidylcholine, which has a stabilizing effect on membranes, constituted almost 50% of the skin phospholipids, with phosphatidyleserine and phsophatidylethanolamine contributing only 13% and 15%, respectively. More importantly, P. schlosseri increased the cholesterol level (to 5.5 micromol g(-1)) and altered the fatty acid composition (increased total saturated fatty acid content) in its skin lipid after exposure to ammonia (30 mmol l(-1) at pH 7.0) for 6 days. These changes might lead to an even lower permeability to NH(3) in the skin, and reduced back diffusion of the actively excreted NH(4)(+) as NH(3) or the net influx of exogenous NH(3), under such conditions.

Acids↗
PubMed2003

Purine derivative excretion in dairy cows: endogenous excretion and the effect of exogenous nucleic acid supply.

An experiment was conducted with dairy cows to study the partitioning of excreted purine derivatives between urine and milk and to quantify the endogenous contribution following the isotopic labeling of microbial purine bases. Three lactating cows in their second lactation that had been cannulated in the rumen and the duodenum were fed a mixed diet (48:52, roughage/concentrate ratio) distributed in equal fractions every 2 h, and duodenal flow of purine bases was determined by the dual-phase marker system. Nitrogen-15 was infused continuously into the rumen to label microbial purine bases, and the endogenous fraction was determined from the isotopic dilution in urinary purine derivatives. Urinary and milk recovery of duodenal purine bases were estimated at early (wk 10) and late (wk 33) lactation by the duodenal infusion of incremental doses (75 and 150 mmol purine bases/d) of RNA from Torula yeast. Each period was 6 d, with RNA being infused during the last 4 d, followed by measurement of the flow of purine bases to the duodenum. The isotope dilution of purine derivatives in urine samples confirmed the presence of an endogenous fraction (512 +/- 36.43 micromol/W0.75 or 56.86 mmol/d) amounting to 26 +/- 3.8% of total renal excretion. Total excretion of purine derivatives in urine plus milk was linearly related to the duodenal input of purine bases, but the slopes differed (P < 0.005) between lactation stages resulting in a lower equimolar recovery in early (y = 58.86 (+/-3.89) +0.56 (+/-0.0164) x; r = 0.90) than late lactation (y = 58.86 (+/-3.89) + 0.70 (+/-0.046) x; r = 0.80). Excretion of purine derivatives through milk represented a minimum fraction of total excretion but responded significantly to the duodenal input of purine bases. No differences between lactation stages were detected, and variations in milk yield did modify significantly the amount of purine derivatives excreted through the milk.

Absorption↗
PubMed1985

[Absorption, distribution, metabolism and excretion of bacmecillinam. I. Absorption, distribution, metabolism and excretion of 14C-bacmecillinam following oral administration to rats].

The pharmacokinetics of bacmecillinam (KW-1100), a new semisynthetic penicillin, was studied. Plasma levels, tissue distribution, metabolites and urinary and biliary excretion of mecillinam after oral administration of KW-1100 were studied in rats given a dose of 20 mg/kg (as mecillinam). The absorption of 14C-KW-1100 was so rapid that the level in blood was found to reach the peak 30 minutes after administration. 14C-KW-1100 was distributed widely into various tissues and relatively high distribution was noted in liver, kidney, adrenal gland and spleen. No accumulation of 14C-KW-1100 in any tissue was found. It was excreted rapidly from each tissue. Within 24 hours after administration of KW-1100, approximately 86% of the given dose was excreted. And within 72 hours, approximately 97% of the dose was excreted. Excretions in urine and feces within 72 hours after KW-1100 administration were 39.5 and 57.4% of the given dose, respectively. Biliary excretion was 2.0% of the given dose within 24 hours after administration of KW-1100. The major metabolite in the plasma at peak time (30 minutes) was mecillinam (50.5%). The major metabolite in the urine (0 approximately 8 hours) was mecillinam (52.2%), too. The minor metabolites were 5,5-dimethyl-2-(1'-formamidomethyl)-thiazolidine-1',4-dicarboxylat e(M-1), 6-beta-[(hexahydro-1H-azepin-1-yl)-methyleneamino]-penicilloic acid (M-6) and M-4.

Administration, Oral↗
PubMedDate not supplied

Triton WR-1339, a lysosomotropic compound, is excreted into bile and alters the biliary excretion of lysosomal enzymes and lipids.

In these experiments, we tested two hypothesis: first, that Triton WR-1339, a nonionic detergent which is sequestered in hepatocyte lysosomes, undergoes biliary excretion; and second, that Triton WR-1339, which also alters serum lipid levels and modifies hepatic catabolism of lipoproteins, affects the biliary output of proteins and lipids. When 3H-Triton WR-1339 was administered to rats, biochemical and morphologic studies showed that hepatocyte lysosomes sequestered Triton WR-1339: (i) the subcellular distribution of 3H was identical to that of lysosomal enzymes after liver fractionation by differential or isopycnic centrifugation, and (ii) lysosomes appeared engorged with Triton WR-1339 on electron microscopy. 3H was also excreted into bile in parallel to three lysosomal enzymes. Triton WR-1339 administration caused a coordinate increase in the biliary excretion of three lysosomal enzymes and also increased the biliary output of total protein, bile acids, and phospholipid. Triton WR-1339 administration did not affect bile flow or the biliary outputs of cholesterol, plasma membrane, and cytosolic enzymes, but did decrease biliary cholesterol saturation by 50%. These results demonstrate that an exogenous compound which is sequestered in hepatocyte lysosomes may be excreted directly into bile in parallel with endogenous lysosomal constituents. The data also show that such a lysosomotropic agent may also selectively modify the biliary excretion of proteins and lipids. The findings are consistent with the existence of a lysosome-to-bile hepatic excretory pathway and suggest that hepatocyte lysosomes may be important in modulating biliary protein and lipid secretion.

Acetylglucosaminidase↗
PubMedDate not supplied

Biliary excretion of copper, manganese, and horseradish peroxidase in Eisai hyperbilirubinemic mutant rats (EHBRs) with defective biliary excretion of glutathione.

A mixture of copper (Cu) (0.38 mg/kg), manganese (Mn (0.038 mg/kg), and horseradish peroxidase (HRP) (5.0 mg/kg) was injected intravenously (i.v.) into mature Eisai hyperbilirubinemic rats (EHBRs) and Sprague-Dawley rats (SDRs). Bile was collected at 10-min intervals before and after the injection, under anesthesia. The liver, kidneys, and blood were removed 40 min after the injection. The serum conjugated bilirubin concentration was 0.85 mg/dL in the EHBRs, but was below detection limits in the SDRs. The bile-reduced glutathione (GSH) concentration was much lower in the EHBRs (0.04 mg/mL) than in the SDRs (1.30 mg/mL). However, the hepatic GSH concentration was about 1.6 times higher in EHBRs (2.26 mg/g liver) than in SDRs (1.43 mg/g liver). The low excretion of biliary GSH was not caused by the activity of GGT in the liver, since there was no significant difference in the activity between the two groups (5.8 +/- 3.4 and 4.6 +/- 2.4 mumol p-nitroaniline/g protein/30 min in SDR and EHBR groups, respectively). There was a delay of initial biliary excretion of Cu in EHBRs compared to SDRs. The biliary concentration of Mn was slightly lower in EHBRs than in SDRs. Forty min after the injection of metals, however, there was no difference between hepatic concentrations of the two metals in the two groups. Our results suggest that abnormal deposition of the two metals is not observed naturally in EHBRs. Injected HRP was excreted rapidly and notably in the EHBRs compared to SDRs. Furthermore, the biliary concentration of beta-N-acetyl-D-glucosaminidase (beta-NAG) was significantly higher in EHBRs than in SDRs, Rapid biliary excretion of Cu, but not of Mn, may be related to the hepatobiliary transport of GSH, but the transport and lysosomal function do not originally regulate the biliary excretion of Cu.

Acetylglucosaminidase↗
PubMed1991

Metabolism of metandienone in man: identification and synthesis of conjugated excreted urinary metabolites, determination of excretion rates and gas chromatographic-mass spectrometric identification of bis-hydroxylated metabolites.

After oral administration of metandienone (17 alpha-methyl-androsta-1,4-dien-17 beta-ol-3-one) to male volunteers conjugated metabolites are isolated from urine via XAD-2-adsorption, enzymatic hydrolysis and preparative high-performance liquid chromatography (HPLC). Four conjugated metabolites are identified by gas chromatography-mass spectrometry (GC/MS) with electron impact (EI)-ionization after derivatization with N-methyl-N-trimethyl-silyl-trifluoroacetamide/trimethylsilyl-imidazole (MSTFA/TMS-Imi) and comparison with synthesized reference compounds: 17 alpha-methyl-5 beta-androst-1-en-17 beta-ol-3-one (II), 17 alpha-methyl-5 beta-androst-1-ene-3 alpha,17 beta-diol (III), 17 beta-methyl-5 beta-androst-1-ene-3 alpha,17 alpha-diol (IV) and 17 alpha-methyl-5 beta-androstane-3 alpha,17 beta-diol (V). After administration of 40 mg of metandienone four bis-hydroxy-metabolites--6 beta,12-dihydroxy-metandienone (IX), 6 beta,16 beta-dihydroxy-metandienone (X), 6 beta,16 alpha-dihydroxy-metandienone (XI) and 6 beta,16 beta-dihydroxy-17-epimetandienone (XII)--were detected in the unconjugated fraction. The metabolites III, IV and V are excreted in a comparable amount to the unconjugated excreted metabolites 17-epimetandienone (VI), 6 beta-hydroxy-metandienone (VII) and 6 beta-hydroxy-17-epimetandienone (VIII). Whereas the unconjugated excreted metabolites show maximum excretion rates between 4 and 12 h after administration the conjugated metabolites III, IV and V are excreted with maximum rates between 12 and 34 h.

Administration, Oral↗
PubMed2006

Urodilatin excretion and its correlation with sodium excretion in healthy full-term newborn infants.

BACKGROUND: Urodilatin (URO) is a member of the natriuretic family, cleaved by the kidney, which acts as a paracrine hormone in the regulation of natriuresis and diuresis. In newborn infants the excretion of urodilatin and its biological effects have not been explored. METHODS: We measured urinary URO excretion, by direct RIA (radioimmunoassay), as well as its correlation to neonatal body weight loss, and sodium homeostasis in 30 full-term newborn infants on the 4th day of life. RESULTS: The URO excretion, estimated as URO:creatinine ratio, was significantly correlated to sodium excretion. CONCLUSION: These data show that in full-term newborn infants the mechanisms that control synthesis, excretion and signal transduction of URO are developed and that URO contributes to natriuresis regulation.

Apgar Score↗
PubMed1997

Enhanced urinary excretion of cGMP in liver cirrhosis. Relationship to hemodynamic changes, neurohormonal activation, and urinary sodium excretion.

Cyclic guanosine monophosphate (cGMP) has been proposed to mediate peripheral arterial vasodilation in liver cirrhosis. Nitric oxide and natriuretic peptides are the main signals for cGMP generation. Variation in urinary cGMP excretion parallels changes in plasma cGMP levels. Our aim was to determine urinary excretion of cGMP (UcGMPV) and to investigate its relationship to systemic hemodynamics, neurohumoral activity and renal sodium excretion in cirrhosis. Urinary excretion of cGMP was measured in 19 healthy subjects and 20 patients with alcoholic cirrhosis. Systemic hemodynamic parameters, blood volume (BV), plasma atrial natriuretic factor (ANF), and the endothelium-dependent vasodilator substance P (SP) were determined in all patients and in five healthy subjects. Urinary cGMPV was higher in the group of patients (736 pg/min; 50-3229 pg/min) than in controls (126 pg/min; 0-1657 pg/min) (P < 0.01). In addition, UcGMPV inversely correlated with the systemic vascular resistance and directly with cardiac output, blood volume, SP, ANF, and Pugh's score. By Cox regression analysis, only systemic vascular resistance remained inversely associated with UcGMPV. In conclusion, urinary cGMP excretion is increased in cirrhosis. It is suggested that increased cGMP generation may be related to the hyperkinetic circulation in human cirrhosis.

Atrial Natriuretic Factor↗
PubMed1986

The importance of renal net acid excretion as a determinant of fasting urinary calcium excretion.

To evaluate the effects of changing rates of fixed acid production on fasting urine Ca/creatinine, we studied five healthy men fed constant diets during control conditions (serum HCO3 27.3 +/- 2.6 SD mEq/liter and blood H+ 40.4 +/- 1.5 microEq/liter) and then during the administration of NH4Cl 3.0 mEq/kg/day (serum HCO3 22.5 +/- 4.9 mEq/liter; P less than 0.025, and H+ 46.8 +/- 2.3 mEq/liter; P less than 0.005). In addition to the expected increase in daily urinary Ca excretion from 5.2 +/- 2.0 to 12.5 +/- 3.0 mmole/day; P less than 0.001 as daily urinary net acid excretion was increased from 48 +/- 32 to 257 +/- 33 mEq/day; P less than 0.001 we observed that fasting urinary net acid/creatinine excretion also increased from 2.9 +/- 1.2 to 11.1 +/- 1.2 mEq/mmole creatinine; P less than 0.001 and fasting urine Ca/creatinine increased from 0.158 +/- 0.111 to 0.456 +/- 0.109 mmole/mmole creatinine; P less than 0.005. The additional Ca appearing in the urine during acidosis ultimately reflected augmented net bone resorption since daily urinary hydroxyproline excretion was increased from 0.232 +/- 0.062 to 0.377 +/- 0.108 mmole/day; P less than 0.01. Since variations in diet composition can cause fixed acid production and thus renal net acid excretion to vary from about zero to 200 mEq/day, such a range could cause fasting Ca/creatinine to vary from 0.09 to 0.37 mmole/mmole (0.03 to 0.13 mg/mg) and should be taken into account in the evaluation of fasting Ca/creatinine.

Acid-Base Equilibrium↗
PubMed1967

Biliary excretion in foreign compounds. Species difference in biliary excretion.

1. The biliary excretion of injected [(14)C]aniline, [(14)C]benzoic acid, 4-amino-hippuric acid and 4-acetamidohippuric acid in six or eight species of animal (rat, dog, hen, cat, rabbit, guinea pig, rhesus monkey and sheep) was studied. 2. These compounds, with molecular weights in the range 93-236, are poorly excreted in the bile in all the species examined and, in effect, there is little significant species difference in the extent of their biliary excretion. 3. Compounds of higher molecular weight (355-495) were also studied, namely succinylsulphathiazole, [(14)C]stilboestrol glucuronide, sulphadimethoxine N(1)-glucuronide and phenolphthalein glucuronide. 4. With these compounds a clear species difference in the extent of biliary excretion was found, the rat, dog and hen being good excretors, the rabbit, guinea pig and monkey poor excretors, and the cat and sheep taking an intermediary position. 5. There was a general trend for biliary excretion to be higher in all species when the compounds were of higher molecular weight. 6. These results are discussed in their relation to species differences in drug metabolism.

Journal Article↗
PubMedDate not supplied

Probenecid markedly reduces urinary excretion of ethinylestradiol and trimethoprim slightly reduces urinary excretion of clenbuterol.

This study investigated whether the illegal application of ethinylestradiol or clenbuterol in cattle as growth promotors may be concealed by co-treatment with drugs that affect urinary excretion. Therefore, six male veal calves were fed with ethinylestradiol and six different male veal calves were fed with clenbuterol for 13 days. Both groups received the growth promotors twice daily (days -2 to 11) with milk replacer. The calves receiving ethinylestradiol were additionally fed with probenecid on days 7-11, and the calves receiving clenbuterol were additionally fed with trimethoprim (days 7-11). During days 1-11 of the experiment, 24-h urine and blood samples (once daily) were collected and analyses for ethinylestradiol and clenbuterol by specific enzyme immunoassay. In four calves the average urinary excretion of ethinylestradiol during days 7-11 (co-treatment with probenecid) was only about 25% of their average urinary excretion of ethinylestradiol on days 1-6. In the other two calves of this group, the excretion of ethinylestradiol was reduced to 4% on days 7-11 compared with days 1-6. In these two calves several urine samples provided concentrations of ethinylestradiol around the limit of detection. As a consequence, there may be a chance of concealing ethinylestradiol application by co-treatment with probenecid. Co-treatment with trimethoprim led only to a slight reduction of urinary excretion of clenbuterol. The detection of clenbuterol in urine samples from calves which were co-treated with trimethoprim can thus not be prevented.

Anabolic Agents↗
PubMed1997

Increased urinary excretion of 3-hydroxyisovaleric acid and decreased urinary excretion of biotin are sensitive early indicators of decreased biotin status in experimental biotin deficiency.

To assess the utility of various indicators of biotin status, marginal biotin deficiency was induced experimentally in normal adults. Ten subjects consumed a diet that contained enough avidin to bind seven times more biotin than that in the diet. Blood and 24-h urine samples were collected before the diet began and twice weekly thereafter for 20 d. The urinary excretion and serum concentration of biotin and its two principal inactive metabolites bisnorbiotin and biotin sulfoxide were determined after HPLC separation with an avidin-binding assay. The urinary concentration of 3-hydroxyisovaleric acid, an indicator of reduced activity of a biotin-dependent enzyme, was quantitated by gas chromatography-mass spectrometry. The urinary excretion of 3-hydroxyisovaleric acid increased significantly (P < 0.0001). For all subjects, the urinary excretion of both biotin and bisnorbiotin decreased significantly (P < 0.0001 for each). In contrast, the mean serum concentration of biotin did not decrease significantly (P = 0.06). These data provide evidence that the urinary excretion of 3-hydroxyisovaleric acid and the urinary excretion of biotin are early and sensitive indicators of biotin deficiency and that the serum concentration of biotin is not.

Adult↗
PubMed1983

Effects of chromium supplementation on urinary Cr excretion of human subjects and correlation of Cr excretion with selected clinical parameters.

Daily urinary chromium (Cr) excretion of 15 healthy free-living female subjects was 0.20 +/- 0.03 microgram (mean +/- SEM) and nearly identical for 27 male subjects, 0.17 +/- 0.02 microgram. Minimum Cr absorption calculated from urinary Cr excretion was about 0.4 percent. Increasing intake fivefold by Cr supplementation led to a nearly fivefold increase in Cr excretion suggesting that the extent of absorption of supplemental inorganic chromium was similar to that from normal dietary sources. Correlations between 24-hour Cr excretion and urine volume, age, total creatinine and body weight were not found. Urinary Cr concentration of samples obtained following a morning void correlated with creatinine and Cr concentration following a glucose challenge but not with serum glucose, insulin, lipid parameters, age or body weight. Similar results were obtained for urine samples obtained from subjects during Cr supplementation. These results suggest that urinary Cr excretion does not appear to be a meaningful indicator of Cr status but is a meaningful indicator of Cr intake and that the absorption of supplemental inorganic Cr was similar to that of Cr from normal dietary sources.

Adult↗