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PubMed1990

Methane excretion and experimental colonic carcinogenesis.

To examine the association between methane (CH4) excretion and experimental colonic carcinogenesis, we measured CH4 excretion in rats treated with the colonic carcinogen azoxymethane (AOM, 7 mg/kg weekly for 10 weeks) and paired controls. CH4 excretion was not initially detected in either experimental or control groups, but all animals acquired positive CH4 excretion status by time of sacrifice (week 26). There was no difference between groups or among AOM-treated animals with and without tumors in the median time to onset of detectable CH4 excretion or in the amount of CH4 excreted. Our results fail to provide support for a link between CH4 excretion and experimental colonic dysplasia or adenocarcinoma.

Adenocarcinoma↗
PubMed1995

[Iodine content in diet and excretion of iodine in urine].

The standard food for our volunteers, prepared in the central kitchen of the University Hospital of Tubingen, consisted of breakfast, warm lunch and cold supper and contained, on average, approximately 230 micrograms of iodine/day. It is generally assumed that an equilibrium is established between iodine intake from food and urinary iodine excretion. Hence, the amount of iodine excreted with the urine within 24 h may reflect the daily ingestion of iodine. The fecal iodine losses are considered negligible. The alimentary iodine supply from food of our clinic would meet the WHO recommendations of > 150 micrograms/day to prevent iodine-deficiency goiters. In 27 healthy volunteers the daily uptake of iodine was determined and the urinary excretion of iodine within 24 h was measured. Unexpectedly, only 16% to 18% of the alimentary iodine were excreted with the urine. Hence, the utilization of iodine from the food appears to be limited and therefore cannot prevent goiters in goiter areas. In addition, it was found that the correlation between urinary excretion of iodine and urinary excretion of creatinine is not a reliable parameter for the real daily excretion of iodine and iodine balance.

Biological Availability↗
PubMed1984

Prostaglandin excretion after furosemide in normal and low-renin essential hypertension.

We examined the urinary excretion of prostaglandin (PG)E2 and PGF2 alpha before and 15 min after stimulation with the acutely vasodilating agent furosemide in 25 normotensive controls and 81 patients with essential hypertension (EH). After furosemide administration, PGE2 excretion was lower in patients with EH (P less than 0.02). Excretion rates of PGF2 alpha and of sodium, and urinary volume in hypertensive patients were not significantly different from the values found in normotensive controls. Patients with low-renin essential hypertension (LREH) had a significantly reduced excretion of both PGE2 and PGF2 alpha before and after administration of furosemide as compared to controls. The difference in PGF2 alpha excretion was also significant when LREH patients were compared to those with normal-renin essential hypertension (NREH). Patients with LREH were older and excreted less potassium than patients with NREH or normotensive controls. We conclude that the reduced PG excretion immediately after furosemide administration in patients with EH reflects a diminished capacity of the hypertensive kidney to generate prostaglandins which exert an overall vasodilating effect. Since renin secretion is under the control of renal PG formation, the decreased responsiveness of plasma renin activity (PRA) observed in patients with EH and predominantly in those with LREH may be the consequence of a decreased renal cortical PG generation. Alternatively, mechanisms that reduce both PRA and PG generation have to be considered.

Adult↗
PubMed1976

[Conditions affecting the renal excretion of manganese by humans (author's transl)].

The renal excretion of manganese is investigated for different urine flow rates in adults of both sexes with normal and disturbed kidney function. Mn is determined by emission spectral analysis. During antidiuresis with a mean urine flow rate of 0,97 +/- 0,66 ml/min (SD) the average excretion of Mn is 11,4 +/- 19,4 ng/min for 1,73 m2 body surface area. With an indifferent urine flow (4,43 +/- 2,11 ml/min) the average Mn excretion is 13,5 +/- 19,3 ng/min. For this type of diuresis Mn excretion and urine flow rate are slightly positively correlated. A further increase in urinary excretion of Mn is observed during osmotic diuresis. In this case 160,6 +/- 180,5 ng Mn/min are eliminated for an urine production of 22,2 +/- 6,8 ml/min. The difference of the mean excretion values is highly significant (P less than 0,01) between indifferent urine flow and osmotic diuresis, insignificant between antidiuresis and indifferent urine flow, and significant (P less than 0,01) between antidiuresis and osmotic diuresis. Down to a clearance value for inulin of less than 30 ml/min and for PAH of less than 200 ml/min and 1,73 m2 body surface area, the Mn excretion is largely independent of the renal hemodynamics.

Adolescent↗
PubMed1982

Metabolism and excretion of the quaternary ammonium compound thiazinamium methylsulfate (Multergan) in man. I. Parenteral administration.

The quaternary ammonium compound thiazinamium was found to be metabolized by sulfoxidation solely. No ring hydroxylation products, nor demethylation products (e.g. promethazine) could be found. Thiazinamium sulfoxide was found both in urine and bile, but thiazinamium is-after parenteral administration - mainly excreted in the unchanged form. After intravenous injection about 40% of the dose was excreted, unchanged, in the urine. The excretion was very rapid and almost complete within eight hours. About 9% of the dose was excreted in the urine in the form of thiazinamium sulfoxide cations. After intramuscular injection virtually the same figures for urinary excretion were found. No correlation could be observed between urine production or pH and the amount of drug excreted in urine. In a study involving bile-fistula patients it was found that both thiazinamium cations and thiazinamium sulfoxide cations are excreted to a considerable extent in bile. The amount of unchanged drug in bile was almost equal to that in urine, but the amount of sulfoxide was slightly higher.

Bile↗
PubMed1995

Mechanisms of biliary excretion of lithocholate-3-sulfate in Eisai hyperbilirubinemic rats (EHBR).

Biliary excretion of lithocholate-3-sulfate is markedly impaired in EHBR. To examine the mechanism of biliary lithocholate-3-sulfate excretion in EHBR, the effects of colchicine treatment, a vesicular transport inhibitor, and infusion of taurocholate and organic anions were studied in EHBR and Sprague-Dawley rats. Colchicine treatment and taurocholate infusion had no effect of biliary lithocholate-3-sulfate excretion in EHBR, suggesting that biliary lithocholate-3-sulfate excretion is not mediated by the vesicular transport or by the bile acid excretory pathway. In control Sprague-Dawley rats, both sulfobromophthalein and dibromosulfophthalein infusion inhibited biliary lithocholate-3-sulfate excretion. In contrast, in EHBR dibromosulfophthalein infusion inhibited biliary lithocholate-3-sulfate excretion but BSP infusion did not. Indocyanine green and pravastatin infusion did not affect biliary lithocholate-3-sulfate excretion but pravastatin infusion had no effect in EHBR. These findings indicate that, whether physiologically important or not, two of more excretory pathways for organic anions exist at the canalicular membrane other than the ATP-dependent one.

Animals↗
PubMed1995

Urinary excretion of retinol-binding protein in healthy children and adolescents.

Retinol-binding protein (RBP) is a marker of tubular reabsorption in the kidneys. The aim of our study was to investigate urinary RBP excretion in healthy children to obtain reference values related to age and pubertal stage. Overnight samples from 143 subjects (73 girls, 70 boys) aged 10-18 years were investigated. RBP was quantified by a solid-phase sandwich enzyme immunoassay. Both the RBP excretion rate and the RBP/creatinine ratio (RBP/Cr) showed a skewed distribution. The medians and the 5th-95th percentiles were 38 ng/min (15-127) and 9 micrograms/mmol (4-23), respectively. The RBP excretion rate and RBP/Cr ratio were similar in both sexes, and linear multiple regression analysis showed no association with age or pubertal stage, although a weak relationship (r = 0.27) was found between RBP excretion rate and age in boys and RBP/Cr ratio and age (r = -0.28) in girls by simple correlation analysis. The correlation between RBP excretion rate and RBP/Cr ratio was 0.76; the RBP excretion rate and RBP/Cr ratio measured on 2 consecutive days, showed a correlation coefficient of 0.84 and 0.88, respectively. We conclude that overnight RBP excretion in children over 10 years shows a low day-to-day variation and, in practical terms, is independent of age, gender and pubertal stage.

Adolescent↗
PubMed1980

Excretion pattern of branched-chain amino acid metabolites during the course of acute infections in a patient with methylmalonic acidaemia.

A 1-year-old boy with a typical B12-responsive form of methylmalonic acidaemia was hospitalized twice due to acute bacterial infections. On both occasions, the child was lethargic with a severe ketoacidosis on admission. Intensive therapy with protein restriction, intravenous administration of electrolytes and antibiotics was effective within 4 days on both occasions. The urinary excretion of organic acids showed the same pattern on both occasions. There were rising excretion concentrations, reaching a peak value within the first 24-hour period, for the following compounds: 3-hydroxybutyric acid, 3-hydroxypropionic acid, 3-hydroxyisobutyric acid and 3-hydroxyisovaleric acid. Excretion concentrations of the following rose for 48 h: isobutyric acid, 2-methylbutyric acid, isovaleric acid, lactic acid and the 2-oxo-acids. There was no increase until 12-24 h after the onset of severe illness in the excretion of propionic acid and methylmalonic acid. Propionic acid excretion was maximal at about 48 h, while peak excretion of methylmalonic acid was delayed until about 72 h after the onset of severe illness; at this time there was clinical improvement. The biochemical implications of this excretion pattern are discussed.

Acute Disease↗
PubMed1993

Relationship between biliary excretion of bilirubin and glutathione disulfide.

The effects of two glutathione-oxidizing agents, t-butyl hydroperoxide and diamide, on biliary excretion of bilirubin and glutathione disulfide were investigated in anesthetized male Sprague-Dawley rats. Bilirubin (unconjugated) was infused at a constant rate of 100 nmol/kg/min through the jugular vein. When biliary excretion of bilirubin was stabilized, either of the glutathione-oxidizing agents was administered via the mesenteric vein. Biliary excretion of glutathione disulfide increased temporarily after the administration and returned to its basal levels within 20 min. The biliary excretion of bilirubin decreased during the same period and returned to the former levels thereafter. Changes in bile flow rates remained within 20% of the basal levels. A linear correlation was found between the increments in the bile concentration of glutathione disulfide and the decrements in that of bilirubin. Furthermore, separate experiments revealed that reduction of hepatocellular glutathione per se had little effect on biliary excretion of bilirubin. The results thus indicate that the reduction of biliary excretion of bilirubin by glutathione-oxidizing agents was due to the increase in biliary excretion of glutathione disulfide, and suggest that a common biliary excretory mechanism is shared, at least partially, by bilirubin and glutathione disulfide in Sprague-Dawley rats.

Animals↗
PubMed1981

Effect of diphenylhydantoin and its main hydroxylated metabolite on the pharmacokinetics and the urinary and biliary excretion of phenobarbital and its p-hydroxy metabolite.

When rats which had been pretreated with a high dose of diphenylhydantoin (80 mg/kg) for 5 days were given a single intravenous dose of phenobarbital (30 mg/kg): (a) There was no increase in the rate at which phenobarbital (PB) disappeared from the plasma or the tissues of pretreated rats. (b) The percentages of phenobarbital and p-hydroxyphenobarbital (free and conjugated) excreted in the urine were similar in both treated and control animals. However, the percentage of conjugated p-hydroxyphenobarbital excreted, was almost twice that of the control group. (c) Pretreatment with diphenylhydantoin (DPH) markedly increased bile flow rates. Therefore these rats excreted more PB than their controls. The biliary excretion of hydroxylated metabolites of PB (free and conjugated), was similar to that found in urine. Hydroxylation was not increased although, there was a significant elevation in the percentage of conjugated metabolite excreted. In a study to establish whether the main metabolites of diphenylhydantoin interfered with the metabolism of phenobarbital the following results were obtained: (a) Intravenous administration of DPH together with PB caused a two-fold increase in the half-life of phenobarbital elimination. (b) Intravenous administration of PB, to bile duct cannulated rats which had been pretreated for 5 days with DPH, caused a significant reduction in the excretion of hydroxylated phenobarbital in comparison with their control group. However, all the excreted DPH was present in the conjugated form. (c) The DPH pretreated rats had significantly lower cytochrome P-450 and mono-oxygenase activities in their hepatic microsomes than the pretreated controls, and higher UDP-glucuronyltransferase activity with DPH itself as the substrate.

Animals↗
PubMed1986

Urinary catecholamine excretion in patients with secondary adrenocortical insufficiency.

To evaluate the relationship between the secretion of cortisol and the activity of adrenal medulla in the secondary adrenocortical insufficiency, the excretion of epinephrine and norepinephrine was documented in 8 patients suffering from panhypopituitarism. Plasma levels and urinary excretion of cortisol were very low in baseline conditions, and the increase in these parameters of cortisol secretion occurring upon ACTH infusion was significantly reduced with respect to the response to ACTH documented in normal subjects. The mean value of urinary epinephrine excretion was at the lower limit of normal values, and a highly significant positive correlation was found between cortisolemia or cortisoluria and urinary epinephrine excretion in these patients. Despite a significant increase in cortisolemia and cortisoluria upon ACTH administration, this acute increase in adrenocortical activity was without any stimulatory effect on epinephrine or norepinephrine excretion. But, as in baseline conditions, a significant correlation was documented for the degree of adrenocortical activity and epinephrine excretion on the day of ACTH administration. It appears, therefore, that in severe secondary adrenocortical insufficiency the excretion of epinephrine is reduced proportionally to the decrease in adrenocortical activity.

Adrenal Insufficiency↗
PubMedDate not supplied

Urinary growth hormone excretion rates in normal and acromegalic man: a critical appraisal of its potential clinical utility.

The assessment of growth hormone (GH) secretory status is often difficult because of the intermittent nature of GH release and resulting wide swings in plasma GH levels. Urinary GH excretion holds promise as an index of integrated plasma GH free of this limitation, but technical problems have prevented its use until recently. We adapted a recently developed method for accurately measuring GH and its various molecular forms in urine to the determination of GH excretion rates. The method involves diafiltration and immunoextraction of GH from urine, with monitoring of recovery and final quantification by radioimmunoassay. Twenty-four h GH excretion rates were determined in 30 normal adults (15 men and 15 women) and 4 acromegalic patients. They ranged from 1 to 81 ng/24 h in men, from 1 to 70 ng/24 h in women and from 87 to 1660 ng/24 h in acromegaly (medians = 8.7, 18.0 and 267 ng/24 h, respectively). Excretion rates varied widely, not only between subjects, but also within the same subject on different days. Women and younger subjects tended to excrete more GH than men and older subjects, although these trends were not statistically significant. Acromegalics excreted significantly more GH than normals (p less than 0.001). Twelve normal subjects underwent simultaneous assessment of 24 h integrated plasma GH (sampling every 20 min) and urine GH excretion. Urine GH correlated weakly (r = 0.45) with integrated plasma GH.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1990

Effects of various metals on hepatic bile calcium excretion in rats: the stimulatory effect of zinc is mediated through acetylcholine action.

The effect of various metals on hepatic bile calcium excretion in rats was investigated. Various metals (0.153 mumol per 100 g body weight) were administered intraperitoneally to rats after cannulation of the bile duct, and the bile was collected for 30 min. Bile calcium excretion was significantly increased by administration of zinc sulfate, cadmium chloride, cobalt chloride, lithium chloride, manganese chloride, and nickel chloride, while it was not altered by strontium chloride and cupric sulfate. Of these metals, the effect of zinc was most remarkable. An appreciable effect of zinc on bile calcium excretion was seen at 7.65 nmol (0.5 micrograms) Zn/100 g, the lowest dose. The stimulatory effect of zinc on bile calcium excretion was completely blocked by the simultaneous administration of verapamil and diltiazem (1.0 mg/100 g), calcium entry blockers, whereas the effects of cadmium and manganese were not prevented by the drugs. Also, the effect of zinc on increasing bile calcium excretion was completely inhibited by treatment with atropine (10 micrograms/100 g). Furthermore, administration of acetylcholine (2 and 5 micrograms/100 g) produced a remarkable elevation of bile calcium excretion. The present investigation demonstrates that zinc can stimulate bile calcium excretion in rats and that the effect may be mediated through acetylcholine action.

Acetylcholine↗
PubMed2003

Urinary excretion of pyridinium cross-links and serum osteocalcin levels in patients with primary high-grade osteosarcoma.

Osteosarcoma is the most frequent primary high grade bone tumor, usually occurring in adolescents and children. The aim of the present study was to investigate parameters of bone turnover as urinary excretion of pyridinoline (Pyr), and deoxypyridinoline (D-Pyr), serum osteocalcin (OC), and total alkaline phosphatase (AP) in patients with osteosarcoma. Thirty-five patients aged 7-22 (median age 14) with primary high-grade osteosarcoma of the extremity entered the study. A control population of age- and sex-matched healthy individuals was studied. Urinary excretion of Pyr, D-Pyr was measured on fasting urine specimens, corrected for creatine excretion (Ucr), and expressed as pM/microM UCr. At the same time as urine collection, blood samples were taken for measurement of AP and OC. In patients with osteosarcoma the urinary excretion of D-Pyr (74.5 +/- 41) was significantly higher (P = 0.005) than in controls (38.2 +/- 22.5). The serum level of OC was significantly lower (P < 0.001) in patients with osteosarcoma than in controls. Moreover, significantly (P = 0.03) higher excretion of D-Pyr (85.3 +/- 43) was found in patients who relapsed after surgical removal of the tumor and chemotherapeutic treatment compared with those (58.1 +/- 22) who remained continuously free of disease. The present study showed significant abnormalities of urinary excretion of pyridinium crosslinks and serum OC level in patients with osteosarcoma. The relation between urinary excretion of D-Pyr and biological tumor aggressiveness observed in the present study requires further investigation.

Adolescent↗
PubMed1998

Genetic and dietary influences on urinary oxalate excretion.

Several genes contribute to the development of calcium oxalate nephrolithiasis as it is a polygenic disease. To explore the influence of genetic factors on oxalate excretion we have examined the distribution of oxalate excretions in 101 normal individuals who consumed self-selected diets. The distribution was apparently trimodal, consistent with the existence of three classes of oxalate excretors reflecting two allelic genes determining high and low oxalate excretion occurring with frequencies of 0.32 and 0.68 respectively. The pattern of inheritance in eight families was compatible with the expression of a pair of codominant alleles. A comparison of the distribution of excretory classes among the 101 normal individuals with that of 101 calcium oxalate stone formers suggests that high oxalate excretion may be associated with a 4-fold increased risk of stone disease and intermediate excretion with a 1.6-fold increase. Control of dietary factors influencing oxalate excretion apparently improved the discrimination between excretory classes in 17 individuals but the intra-individual variability in oxalate excretion was not reduced in four of nine individuals in whom this parameter was evaluated. More stringent dietary control than that applied in this study may be required before more extensive genotyping of individuals is attempted.

Adult↗
PubMed2004

Urine mesna excretion after intravenous and oral dosing in ifosfamide-treated children.

PURPOSE: To describe mesna excretion in children. PATIENTS AND METHODS: We studied 14 children (aged 1-18 years) who received 1.8 g/m(2) of ifosfamide per day for 5 days. For uroprotection, the children were given intravenous mesna (equal to 20% of the ifosfamide dose) followed by two oral doses (each equal to 40% of the ifosfamide dose). The concentrations of mesna and the metabolite dimesna were measured in urine samples collected on treatment days 1 and 5. RESULTS: Of 14 patients enrolled, 11 (aged 4-18 years) were evaluable. The profiles of mesna excretion rates were similar on days 1 and 5. Mesna excretion declined rapidly over 1-2 h after intravenous dosing. Increases in mesna excretion after oral dosing lagged by 2-4 h. About 21% of the mesna administered was excreted unchanged over 24 h on both days 1 and 5. The proportion excreted varied by severalfold between patients, but there was no association with age. CONCLUSION: The profile of mesna excretion after intravenous and oral dosing in these children was similar to that in reported studies of ifosfamide-treated adults.

Administration, Oral↗
PubMed1997

Urinary excretion of dimethylhippuric acids in humans after exposure to trimethylbenzenes.

The aim of this study was to determine the urinary excretion of dimethylhippuric acids (DMHAs) in humans after experimental chamber exposure to trimethylbenzene (TMB) vapor. The DMHAs have been put forward as suitable biomarkers of exposure to products containing TMBs such as white spirit and petrol. Ten healthy male volunteers were exposed to TMB vapor in an exposure chamber for 2 h at a work load of 50 W. The subjects were exposed on four occasions, to 25 ppm of 1,2,4-TMB, 1,2,3-TMB, and 1,3,5-TMB, respectively, and 2 ppm of 1,2,4-TMB. Urine was collected from the onset of exposure until the following morning. All six possible DMHA isomers were analyzed by high-performance liquid chromatography. About 22% of the inhaled amount of 1,2,4-TMB was excreted as DMHAs within 24 h, mainly as 3,4-DMHA. The 24-h recovery of 1,2,3-TMB as DMHAs was 11%. Only 3% of the absorbed amount of 1,3,5-TMB was excreted as 3,5,-DMHA. The half-times of the different DMHA isomers ranged from 4 to 16 h. In addition to analysis of DMHAs, the excretion of unconjugated dimethylbenzoic acids in urine was estimated to account for approximately 3% of the dose of all TMBs. In conclusion, the urinary excretion of DMHA isomers may serve as a good indicator of TMB exposure. In this controlled short-term-exposure study the sum of excretion rate of several DMHA isomers reflected exposure more closely than did the excretion rate of any single DMHA.

Adult↗
PubMed2006

Unchanged expression of the sodium-dependent phosphate cotransporter NaPi-IIa despite diurnal changes in renal phosphate excretion.

Renal phosphate excretion is subjected to circadian rhythmicity. The bulk of filtered inorganic phosphate (P(i)) is reabsorbed by the sodium-dependent phosphate cotransporter NaPi-IIa. The regulation of proximal tubular phosphate reabsorptive capacity is largely attributed to the altered abundance of NaPi-IIa residing in the brush border membrane (BBM) of proximal tubular cells. Therefore, we examined if the diurnal rise in renal phosphate excretion is accompanied by a corresponding change in NaPi-IIa expression. Renal phosphate excretion, creatinine clearance, and serum phosphate were determined at consecutive time points in rats, starting from 8 a.m. until 5 p.m. During this period, renal phosphate excretion (fractional P(i) excretion) increased more than eightfold until 5 p.m. compared to the morning values at 8 a.m. In addition, serum phosphate and creatinine clearance as well as the calculated tubular phosphate threshold increased. Neither immunoblot analysis of BBMs nor immunohistochemical staining for NaPi-IIa yielded evidence for a lower abundance of NaPi-IIa in kidneys collected in the afternoon compared to those in the morning. However, kidneys sampled in the afternoon showed a small decrease (14%) in (32)P uptakes into BBM vesicles (BBMVs). Thus, the diurnal rise in renal phosphate excretion was associated with a mild reduction in the sodium-dependent phosphate transport rate in proximal tubular BBMs. There was no apparent downregulation of NaPi-IIa abundance and only a small reduction in Na(+)-dependent Pi-transport activity. Thus, the diurnal changes in urinary phosphate excretion appear to be mainly related to changes in serum phosphate and tubular threshold but not to NaPi-IIa expression.

Algorithms↗