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PubMed1996

Geographical and temporal differences in the urinary excretion of inorganic arsenic: a Belgian population study.

OBJECTIVE: This Belgian study assessed the geographical and temporal differences in the exposure of the population to inorganic arsenic, a known carcinogen. METHODS: In the CadmiBel study (1985-9) the 24 h urinary arsenic excretion was measured, as an index of recent exposure, in industrialised cities (Liège: n = 664, Charleroi: n = 291), in a rural control area (Hechtel-Eksel: n = 397), and in rural districts in which the population had possibly been exposed through the drinking water or the emissions of nonferrous smelters (Wezel: n = 93, Lommel: n = 111, and Pelt: n = 133). In the PheeCad study, in 1991-5, the rural areas (n = 609) were re-examined together with an urban control area (Leuven: n = 152). RESULTS: The CadmiBel results showed that after adjustment for sex, age, and body mass index, the 24 h arsenic excretion was on average low in Liège (91 nmol), Charleroi (155 nmol), Hechtel-Eksel (144 nmol), and Wezel (158 nmol), whereas the highest excretions were found in Lommel (570 nmol) and Pelt (373 nmol). During the PheeCad study, the mean 24 h arsenic excretion in the rural areas ranged from 81 to 111 nmol. This was lower than six years earlier and similar to the excretion in the control town (108 nmol). Longitudinal studies in 529 people living in the rural areas confirmed that their 24 h arsenic excretion had decreased (P < 0.001) from 222 to 100 nmol. As well as the drinking water, industry was likely to be a source of the increased exposure in Lommel and Pelt in 1985-9, because at that time the urinary arsenic excretion did not follow the regional differences in the arsenic content of the drinking water, because the fall in the arsenic excretion over time coincided with the implementation by industry of stricter environmental regulations, because in individual subjects the urinary arsenic excretion was inversely correlated with the distance to the nearest smelter, and because an increased arsenic excretion was only found downwind from the main smelter. The official network that monitors the arsenic concentration in airborne and fall out dust did not detect the high exposure in Lommel and Pelt between 1985 and 1989. CONCLUSION: This study highlights the necessity to validate environmental monitoring programmes by directly estimating the internal exposure of the population.

Adult↗
PubMed1987

Age-dependent biliary excretion of glutathione-related thiols in rats: role of gamma-glutamyltransferase.

The role of gamma-glutamyltransferase (GGT) in the biliary excretion of glutathione (GS) was studied in rats during postnatal development. Between 2 and 10 wk of age the biliary excretion of GS-related sulfur increased ninefold. During this period, alterations were observed in both hepatic GGT and the composition of GS-related thiols and disulfides in bile. For instance, between 3 and 4 wk of age, GGT activity and the biliary excretion of GS hydrolysis products (Cys-Gly and Cys) increased markedly, and the latter became the predominant sulfhydryls in bile. However, by 10 wk of age, the excretion rate of GS increased and exceeded the rate of excretion of Cys-Gly and Cys. The parallelism between hepatic GGT activity and the biliary excretion of GS-hydrolysis products during development suggests a role for GGT in the formation of biliary Cys-Gly and Cys. Furthermore, in 4-wk-old rats, inhibition of hepatic GGT by acivicin markedly decreased the biliary excretion of Cys-Gly and Cys and increased that of GS without influencing the excretion of total GS-related sulfur in bile. The biliary excretion of GS-related thiols was less responsive to acivicin in 2- and 7- to 10-wk-old rats, suggesting that GGT plays a smaller role in influencing biliary thiol composition at those ages. In summary, GS transported into bile is hydrolyzed in an age-dependent manner, however, the GGT-initiated hydrolysis of GS does not affect the biliary excretion of total thiols in rats.

Aging↗
PubMed1988

Homeostatic potassium excretion in fed and fasted sheep.

In unanesthetized adult sheep, following intake of a daily meal, there was a peak in K excretion. The maximum and minimum rates of K excretion following meals were directly related to meal K content. On days without meals, no peak in K excretion occurred. Changes in K excretion on fed and fast days occurred without changes in the low levels of plasma aldosterone and were poorly correlated with urine or blood pH, urine flow rate, Na excretion, or the filtered load of K, but they correlated well with fractional K excretion. Plasma K did not change on fast days. Plasma K increased on some, but not all, fed days. Increases in plasma K that occurred on fed days were insufficient to account for the concurrent kaliuresis. Infusion of aldosterone or isotonic NaCl failed to alter K excretion in fed or fasted sheep. Infusion of isotonic NaCl + aldosterone hypertonic Na2SO4 + aldosterone increased K excretion in fasted but not fed sheep. Infusion of K in the rumen of fed and fasted sheep elevated rumen K concentration and led to increases in K excretion that could not be explained by increases in plasma K. The mechanisms responsible for the homeostatic changes in K excretion on fed and fast days were not ascertained but may importantly depend on sensors of enteric K content.

Aldosterone↗
PubMed1996

Postprandial natriuresis in humans: further evidence that urodilatin, not ANP, modulates sodium excretion.

We examined the effects of a high-salt (100 mmol NaCl) and a low-salt (5 mmol NaCl) meal on the renal excretion of sodium and chloride in 12 healthy male upright subjects. We also measured the urinary excretion of urodilatin [ANP-(95-126)], and the plasma or serum concentrations of atrial natriuretic peptide [ANP-(99-126)], aldosterone, and renin. The high-salt meal produced a postprandial natriuresis (urinary sodium excretion from 59.0 to a peak rate of 204.6 mumol/min in 3rd h after ingestion of meal) and chloride excretion. In parallel, the urinary excretion of urodilatin increased from 35.7 to a peak rate of 105 fmol/min. The effect of high-salt intake on urinary sodium, chloride, and urodilatin excretion was significant (analysis of variance, P < 0.01), and close significant correlations were observed between urodilatin and sodium excretion (mean R = 0.702) as well as between urodilatin and chloride excretion (mean R = 0.776). In contrast, plasma ANP, which was acutely elevated 15 min after high-salt intake, was already back to low-salt values 1 h later. It did not parallel the postprandial natriuretic profile, and no positive correlation between plasma ANP and sodium excretion was observed. These results provide further evidence that urodilatin, not ANP, is the member of this peptide family primarily involved in the regulation of the excretion of sodium and chloride.

Aldosterone↗
PubMed1999

Excretion of tamm-horsfall protein in patients with uric acid stones.

The cause of reduced Tamm-Horsfall protein excretion in patients suffering from uric acid diathesis is still unknown. Our investigation was conducted based on the hypothesis that the solubility of uric acid is increased by Tamm-Horsfall protein and that an increased uric acid content in the urine might cause a decrease in Tamm-Horsfall protein. In 20 patients with uric calculi the excretion of Tamm-Horsfall protein, uric acid, calcium, and citrate was measured. 65% of the patients had pure uric acid stones (group I) and 35% showed mixed stones with at least 30% of uric acid (group II). Reduced Tamm-Horsfall protein excretion was found in 63% of the patients of group I and in 43% of the patients of group II. The excretion of Tamm-Horsfall protein was significantly reduced in pure uric acid stone formers compared to normal subjects (p < 0. 0001). The excretion of uric acid was elevated in 61% of the patients of group I and in 86% of the patients of group II. There was no significant correlation between Tamm-Horsfall protein excretion and uric acid excretion (r = 0.2139). Calcium excretion was elevated in 57% of the patients with mixed stones. The excretion of citrate was reduced in almost all of the patients of groups I and II. Our results do not support the hypothesis that an increased content of uric acid in the urine causes a decrease in Tamm-Horsfall protein. In our opinion the lower excretion of Tamm-Horsfall protein in some of the stone patients might be caused by damage in the distal tubular epithelium. Moreover, it has to be supposed that there are defects both in the distal and the proximal tubule in patients prone to develop uric acid calculi.

Albuminuria↗
PubMed2002

Urinary sodium and potassium excretion in idiopathic hypercalciuria of children.

BACKGROUND: An increased spot urine Na/K ratio (UNa/K) has been found to be related to urinary stone disease in adults with a history of nephrolithiasis and in children with idiopathic hypercalciuria (HC). However, the respective role played by Na and K excretion in the rise of the UNa/K in growing individuals is not well clarified. METHODS: The urinary excretion of Na and K was evaluated in fasting morning and 24-hour urine samples of 37 consecutive children with HC and of 21 previously HC children who were normocalciuric at the time of the study (ExHC). None of them had received any dietary or specific drug prescription. RESULTS: In the HC and in the ExHC group, respectively, the Na excretion was 4 +/- (SD) 2.4 and 2.9 +/- 1.3 mmol/kg/day (p = 0.009); the K excretion was 1.1 +/- 0.4 and 1.2 +/- 0.7 mmol/kg/day (p = 0.86); the fasting UNa/K was 3 +/- 1.6 and 2.1 +/- 1 mmol/mmol (p = 0.044), and the 24-hour UNa/K was 4.2 +/- 3.9 and 2.8 +/- 1.5 mmol/ mmol (p = 0.045). The 24-hour UNa/K was significantly higher than the fasting UNa/K in both HC (p = 0.002) and ExHC (p = 0.002) subjects. The 24-hour UNa/K significantly increased with age in both HC (p = 0.02) and ExHC (p = 0.015) children. The K excretion significantly decreased with age in HC (p = 0.0001) and ExHC (p = 0.005) subjects, as well as with body weight gain in HC (p = 0.005) and ExHC (p = 0.0001) children and with increasing body height in HC (p = 0.006) and ExHC (p = 0.001) subjects. In neither group was the K excretion significantly related to body mass index Z score nor to height Z score. No significant relation resulted between Na excretion and age, body weight and height, and body mass index Z score and height Z score. CONCLUSIONS: HC children have a higher Na excretion as well as a higher fasting and 24-hour UNa/K than ExHC children, but no different K excretion. Meals are accompanied by a significant rise in UNa/K. The rise in UNa/K with age is mostly due to a decrease in K excretion which possibly depends on childhood body growth.

Adolescent↗
PubMed1984

Urinary excretion, osmolarity and electrolytes after bolus-injection of fenoterol in female rabbits.

The effects of bolus injections of 1.0-80.0 micrograms/kg body weight fenoterol on urinary excretion, osmolarity and electrolytes were studied in unanesthetized, water-loaded rabbits. In animals infused initially with isotonic solution over 2 h with 60 ml/h and thereafter over 10 h with 45 ml/h, urine excretion was 538 ml/12 h, sodium excretion was 65.4 mmol/12 h, and potassium excretion was 4.8 mmol/12 h. In animals injected with 5.0-80.0 micrograms/kg body weight fenoterol, a strong antidiuresis occurred, lasting for 2 (10.0 micrograms/kg) to 4 h (80.0 micrograms/kg). Due to the strong antidiuresis, urinary osmolarity was significantly elevated for 2 (10.0 micrograms/kg) to 3 h (80.0 micrograms/kg). The changes of sodium excretion after fenoterol injection were very similar to those of urine excretion. Maximum reduction of sodium excretion was found after injection of 10.0-80.0 micrograms/kg body weight fenoterol, the effect lasting for 1 h (10.0 micrograms/kg) to 4 h (80.0 micrograms/kg). Potassium excretion was significantly reduced after injection of 5.0-80.0 micrograms/kg body weight fenoterol. In contrast to all the other parameters measured, potassium excretion remained significantly reduced until the end of the infusion period in animals treated with 10.0-80.0 micrograms/kg body weight fenoterol and was not dose dependent. Our data presented in this work extend earlier findings in the rabbit in that bolus injection of fenoterol also results in a drastic decrease of urine and electrolyte excretion. The results are discussed with special reference for the management of acute fetal distress with betamimetics and to the development of pulmonary edema that has been shown to occur under therapy with betamimetics on both female rabbits and humans.

Animals↗
PubMed2006

Predictors of angiotensin-converting enzyme inhibitor-induced reduction of urinary albumin excretion in nondiabetic patients.

Urinary albumin excretion is a predictor for cardiovascular mortality and morbidity. We investigated which parameters determine baseline urinary albumin excretion in nondiabetic subjects, without renal disease. In addition, we evaluated the parameters that predict the albuminuria-lowering efficacy of an angiotensin-converting enzyme inhibitor. In this substudy of the Prevention of Renal and Vascular Endstage Disease Intervention Trial, 384 microalbuminuric patients were included. Patient and biochemical characteristics were obtained at baseline and after 3 months of double-blinded, randomized treatment (fosinopril 20 mg or placebo). Mean age was 51.1+/-11.5 years, and 65.6% were male. Median urinary albumin excretion was 22.2 mg per 24 hours. At baseline, mean arterial pressure (beta(standardized)=0.161; P=0.006), urinary sodium excretion (beta(standardized)=0.154; P=0.011), and estimated renal function were independently associated with albumin excretion. In these predominantly normotensive to prehypertensive subjects, fosinopril reduced albumin excretion by 18.5% versus a 6.1% increase on placebo after 3 months (P<0.001). Fosinopril use and blood pressure reduction independently predicted the change in urinary albumin excretion. Baseline urinary albumin excretion independently predicted the antialbuminuric effect of fosinopril (beta(standardized)=-0.303; P<0.001). In conclusion, at baseline, sodium intake and blood pressure were positively associated with urinary albumin excretion. Fosinopril reduced albuminuria more than might be expected from its blood pressure-lowering effect alone, and this effect was more outspoken in subjects with higher baseline albumin excretion. Based on our data, we hypothesize that angiotensin-converting enzyme inhibition may result in superior cardiovascular protection when compared with other blood pressure-lowering agents in subjects with higher baseline levels of albuminuria.

Albuminuria↗
PubMed1982

The effect of dexamethasone on renal electrolyte excretion in the adrenalectomized rat.

The acute effect of low and high doses of dexamethasone on renal electrolyte excretion was examined in chronically (2--3 weeks) adrenalectomized rats and was compared with that of aldosterone. At the lowest effective dose (2 micrograms/100 g BW) dexamethasone injection produced a 70% increase in urinary potassium (K) excretion (0.99 +/- 0.06 to 1.70 +/- 0.20 mueq/min; P less than 0.005) but had no effect on sodium excretion. In contrast, low doses of aldosterone (2.5 micrograms/100 g BW) caused a significant decrease in urinary sodium excretion (6.23 +/- 1.2 to 2.75 +/- 0.7 mueq/min; P less than 0.01) but had no influence on renal potassium excretion (UKV). Higher doses of dexamethasone (10, 20 and 50 micrograms/100 g BW) produced a greater kaliuresis, increasing UKV by more than 100% over baseline and higher (P less than 0.05) than values after a low dose of dexamethasone, but again failed to lower sodium excretion. The increase in UKV after all doses of dexamethasone occurred in association with a significant increase in urinary K concentration; at higher doses of dexamethasone there was a variable increase in urine flow. The increase in UKV was not secondary to an increase in plasma K concentration nor was it associated with a rise in blood pressure or glomerular filtration rate after dexamethasone administration. These findings demonstrate that, in the adrenalectomized rat, acute administration of low and high doses of dexamethasone increases urinary K excretion without affecting sodium excretion. In contrast, aldosterone has little effect on K excretion but significantly decreases sodium excretion. These results indicate that the kaliuresis observed after dexamethasone cannot be attributed to a mineralocorticoid property of the hormone.

Adrenalectomy↗
PubMed1975

Urinary excretion of adenosine 3',5'-monophosphate and guanosine 3',5'-monophosphate in normal children and those with cystic fibrosis.

The urinary excretion of adenosine 3',5'-monophosphate (cyclic AMP) and guanosine 3',5'-monophosphate (cyclic GMP) was examined in 98 normal children and 46 children with cystic fibrosis between the ages of 9 months and 18 yr. Diurnal variations in cyclic AMP and cyclic GMP excretion were observed in subjects from either group, and peak levels of cyclic nucleotide excretion were generally observed during the period of 0700 to 2100 h. Excretion rates (mumol/day) of cyclic AMP and cyclic GMP increased significantly with age. When cyclic AMP and cyclic GMP excretion rates were normalized for urinary creatine, or body weight, the values declined significantly with age in both groups of patients. Cyclic GMP excretion normalized for body surface area also decreased with age, while the value for cyclic AMP (2.86 plus or minus 0.08 mumol/day/m2, mean plus or minus SE) was constant with age in both normals and cystic fibrosis children. With some comparisons of age groups there were significant differences in cyclic nucleotide excretion between normal subjects and children with cystic fibrosis. The differences noted were dependent upon the methods used to normalize excretion rates (urinary creatine, body weight, surface area, and the ratio of cyclic AMP to cyclic GMP excreated). In general patients with cystic fibrosis excreted greater amounts of cyclic GMP than did normals. The most striking comparison was the ratio of cyclic AMP to cyclic GMP excreted which was 9.09 plus or minus 0.50 in all normal children and 4.41 plus or minus 0.32 in children with cystic fibrosis (P smaller than 0.001).

Adolescent↗
PubMed1981

Urinary tetrahydroaldosterone and aldosterone-18-glucuronide excretion in white and black normal subjects and hypertensive patients.

Urinary aldosterone excretion is commonly determined by assay of aldosterone liberated from the acid-labile metabolite, aldosterone-18-glucuronide (Aldo-18-G), which reflects 5-15% of aldosterone secretion. However, since 3alpha, 5beta-tetrahydroaldosterone (TH-Aldo), the major metabolite, reflects 15-40% of aldosterone excretion, determination of its excretion should usually provide a more accurate index of aldosterone secretion. We have validated a RIA for urinary TH-Aldo and compared its excretion in black and white normal subjects and patients with essential hypertension and primary aldosteronism during consumption of low, normal, and high sodium diets. Urinary TH-Aldo excretion averaged 4.5 +/- 2.0 (mean +/- SD) times that of Aldo-18-G. The ratio of excretion of the two remained relatively constant during low, normal, and high sodium diets. There was no difference in the excretion of TH-Aldo or Aldo-18-G in black vs. white normal subjects or hypertensive patients and no age-related changes in the excretion of either metabolite from 20-60 yr of age. Two of nine patients with primary aldosteronism had normal Also-18-G excretion but elevated TH-Aldo excretion. We conclude that determination of both metabolites increases the diagnostic accuracy for primary aldosteronism.

Adult↗
PubMed2001

Close association of urinary excretion of aquaporin-2 with appropriate and inappropriate arginine vasopressin-dependent antidiuresis in hyponatremia in elderly subjects.

The present study was undertaken to determine whether urinary excretion of aquaporin-2 (AQP-2) participates in the involvement of arginine vasopressin (AVP) in hyponatremia less than 130 mmol/L in 33 elderly subjects (> or =65 yr old) during the last 5-yr period. Subjects were separated into euvolemic hyponatremia groups: 13 with hypopituitarism, 8 with syndrome of inappropriate secretion of antidiuretic hormone (SIADH), 8 with mineralocorticoid-responsive hyponatremia of the elderly, and 4 with miscellaneous diseases. Approximately 40% of those with hyponatremia was derived from hypopituitarism, but severe hyponatremia was found in the patients with SIADH and mineralocorticoid-responsive hyponatremia of the elderly. Plasma AVP levels remained relatively high despite hypoosmolality and were tightly linked with exaggerated urinary excretion of AQP-2 and antidiuresis in the 3 groups of patients, except for one miscellaneous one. An acute water load test verified the impairment in water excretion, because the percent excretion of the water load was less than 42% and the minimal urinary osmolality was not sufficiently diluted. Also, plasma AVP and urinary excretion of AQP-2 were not reduced after the water load. The inappropriate secretion of AVP was evident in the patients with SIADH and hypopituitarism, and hydrocortisone replacement normalized urinary excretion of AQP-2 and renal water excretion in those with hypopituitarism. In contrast, the appropriate antidiuresis seemed to compensate loss of body fluid in the patients with mineralocorticoid-responsive hyponatremia of the elderly, who lost circulatory blood volume by 7.3% (mean). Fludrocortisone acetate increased renal sodium handling and body fluid, resulting in the reduction in AVP release and urinary excretion of AQP-2 in mineralocorticoid-responsive hyponatremia of the elderly. These findings indicate that urinary excretion of AQP-2 may be a more sensitive measure of AVP effect on renal collecting duct cells than are plasma AVP levels, and that increased urinary excretion of AQP-2 shows exaggerated AVP-induced antidiuresis in hyponatremic subjects in the elderly. In addition, mineralocorticoid-responsive hyponatremia of the elderly has to be carefully differentiated from SIADH in elderly subjects.

Aged↗
PubMed1991

Adrenergic inhibition of carbon dioxide excretion by trout red blood cells in vitro is mediated by activation of Na+/H+ exchange.

We have used a sensitive new technique to assess the mechanism(s) of adrenergic inhibition of rainbow trout (Oncorhynchus mykiss) red blood cell (RBC) carbon dioxide excretion in vitro. The effect was only apparent using blood acidified to simulate metabolic acidosis. Red blood cell CO2 excretion was inhibited in a dose-dependent manner by physiologically relevant concentrations of noradrenaline (10-1000 nmol l-1) or adrenaline (100-1000 nmol l-1). The beta-adrenoceptor antagonist propranolol abolished the inhibitory effect of adrenaline, whereas the alpha-adrenoceptor antagonist phentolamine was without effect. The action of noradrenaline on RBC CO2 excretion was mimicked by the beta-adrenoceptor agonist isoproterenol, but not by the alpha-adrenoceptor agonist phenylephrine. Therefore, adrenergic inhibition of CO2 excretion is mediated by RBC beta-adrenoceptors, presumably of the beta 1 subtype. The Na+/H+ exchange inhibitor amiloride effectively blocked adrenergic stimulation of Na+/H+ exchange (as indicated from measurements of pHe and RBC pHi) and entirely prevented the inhibition of CO2 excretion. Noradrenaline significantly reduced the rate of CO2 excretion even in the presence of the Cl-/HCO3- exchange inhibitor SITS. Therefore, adrenergic inhibition of CO2 excretion is accomplished via activation of RBC Na+/H+ exchange rather than by a direct inhibition of Cl-/HCO3- exchange. The observed relationship between CO2 excretion rates and the RBC transmembrane pH difference (pHe-pHi) and the occurrence of the inhibition only at low pHe provide further evidence of the linkage with RBC Na+/H+ exchange. We suggest that adrenergic activation of RBC Na+/H+ exchange impedes CO2 excretion by causing a rise in intracellular HCO3- levels concurrent with a reduction of intracellular PCO2. The net result is a reduced gradient for HCO3- entry into the RBC in conjunction with a diminution of the outwardly directed PCO2 gradient. Thus, the rate of formation of CO2 from the dehydration of plasma HCO3- is reduced and, in turn, a portion of this CO2 is not excreted but recycled through the red blood cell.

Adrenergic Antagonists↗
PubMed1989

Urinary orosomucoid excretion rate in patients with non-insulin-dependent diabetes mellitus.

Urinary excretion rate and clearance of alpha 1-acid glycoprotein (orosomucoid), a major serum glycoprotein which is more anionic (pI 2.7) than albumin (pI 4.7) were measured by RIA in timed overnight urine samples from non-insulin-dependent diabetic patients with different urinary albumin excretion rate and from healthy controls. The 50th percentiles of urinary orosomucoid excretion rate in patients with normo-, micro-, and macroalbuminuria were larger than those in healthy controls. Urinary excretion rate and clearance of orosomucoid increased in parallel with increase in albumin excretion rate in diabetic patients with an albumin excretion rate of more than 10 micrograms/min. On the basis of their levels of urinary orosomucoid excretion, patients with normoalbuminuria of less than 10 micrograms/min could be divided into two groups, one with a normal and the other with an elevated urinary orosomucoid excretion rate. The findings suggest that kidneys of diabetic patients with an albumin excretion rate of more than 10 micrograms/min are unable to distinguish the difference in pI between albumin and orosomucoid, and that a subgroup with an elevated orosomucoid excretion rate may be present among diabetics with normoalbuminuria.

Adult↗
PubMed1985

[Urinary excretion of cadmium, copper and zinc in workers exposed to cadmium].

Changes in urinary cadmium, copper and zinc excretion in workers who had considerable exposure to cadmium oxide fumes were investigated over a 5-year period following the cessation of exposure. The 22 male subjects aged 22 to 55 had been welders on automobile parts for periods ranging from 7 months to 23 years, using silver solder which contained cadmium. They were divided into three groups according to levels of urinary cadmium in the first medical examination in 1975: 5 in the high excretion group, 11 in the moderate group, and 6 in the low group. Renal tubular dysfunctions were indicated in most workers in the high excretion group but not in the other two groups. The high and moderate groups showed a rapid decrease in the levels of urinary-excreted cadmium, with biological half-times of 1.42 and 1.21 years, respectively. Excreted cadmium levelled off in the two groups about 1.7 and 1.5 years after the last exposure. Urinary copper excretion in the high cadmium excretion group was about twice that in the moderate and low groups, the difference being statistically significant in comparison with the controls. Urinary zinc excretion was high in all subjects immediately after cessation of exposure but decreased rapidly. After three years it was found that the reduction of urinary zinc was greatest in the high cadmium group. Urinary cadmium showed significant correlations with both copper and zinc. Urinary copper showed a negative correlation with zinc excretion in the high cadmium excretion group and a significant positive correlation in the other two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Effects of dietary protein and oathull fiber on nitrogen excretion patterns and postprandial plasma urea profiles in grower pigs.

The objectives of this study were: 1) to determine if dietary protein reduction or oathull fiber inclusion would reduce urinary N excretion in grower pigs, 2) to determine if plasma urea could predict urinary N excretion among diets differing in protein and fiber content with an expected range in N excretion patterns, and 3) to determine the postprandial time point to sample blood for the best prediction. Three dietary protein concentrations (high, 19.7; medium, 16.9; low, 13.8%) and two fiber levels (high, 5.0; low, 3.6% crude fiber) were tested in a 3 x 2 factorial arrangement. Diets (wheat, barley, soybean meal; oathulls as fiber source) were formulated to 3.25 Mcal of digestible energy (DE)/kg and 2.2 g of digestible lysine/Mcal DE for low- and medium-protein diets, and 2.4 g/Mcal of DE for high-protein diets, and supplemented with lysine, methionine, tryptophan, threonine, isoleucine, or valine to meet an ideal amino acid profile. Pigs (32 +/- 3.4 kg; n = 42) were housed in metabolism crates for 19 d. On d 10 or 11, catheters were installed by cranial vena cava venipuncture. Daily feeding allowance was adjusted to 3x maintenance (3 x 110 kcal DE/kg body weight(0.75)), and was fed in two equal meals. Feces and urine were collected from d 15 to 19. Five blood samples were collected in 2-h intervals on d 16 and 19. Fecal, urinary, and total N excretion was reduced linearly with a reduction of dietary protein (P < 0.001); the reduction was greater for urinary (48%) and total N excretion (40%) than for fecal N excretion (23%). Similarly, the ratio of urinary to fecal N was reduced linearly with a reduction of dietary protein (P < 0.001). Retention of N (g/d) was reduced linearly, but N retention as a percentage of N intake was increased linearly with a reduction of dietary protein (P < 0.001). The addition of oathulls did not affect N excretion patterns and plasma urea (P > 0.10). Dietary treatments did not affect average daily gain or feed efficiency (P > 0.10). A dietary protein x time interaction affected plasma urea (P < 0.001). For medium- and high-protein diets, plasma urea increased postprandially, peaking 4 h after feeding, and then decreased toward preprandial levels (P < 0.05). Plasma urea did not alter postprandially for the low-protein diet (P > 0.10). Urinary N excretion (g/d) was predicted by 3.03 + 2.14 x plasma urea concentration (mmol/L) at 4 h after feeding (R2 = 0.66). Plasma urea concentration is indicative of daily urinary N excretion and reduction of dietary protein is effective to reduce total and urinary N excretion.

Animals↗
PubMed1988

Human dose-excretion studies with pyrethroid insecticides cypermethrin and alphacypermethrin: relevance for biological monitoring.

1. Dose-excretion studies with cypermethrin (as a 1:1 cis/trans mixture) and alphacypermethrin (one of the two disastereoisomer pairs which constitute cis cypermethrin) were carried out with, in each case, two volunteers per dose level. The studies included (a) single oral alphacypermethrin doses of 0.25 mg, 0.50 mg and 0.75 mg followed by repeated alphacypermethrin doses at the same levels, daily for five days, (b) repeated oral cypermethrin doses of 0.25 mg, 0.75 mg and 1.5 mg daily for five days, and (c) a single dermal application of 25 mg cypermethrin to the forearm. Urine was monitored for the free and conjugated 3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylic acid before and after dosing. 2. Metabolism and rate of excretion of a single oral dose of alphacypermethrin was similar to that of cis cypermethrin, on average, 43% of the dose was excreted as the cyclopropanecarboxylic acid in the first 24 h urine. There was no increase in urinary metabolite excretion when alphacypermethrin was administered as a repeated oral dose. Subjects excreted, on average, 49% of the dose as the cyclopropanecarboxylic acid in the subsequent 24 h periods after dosing. 3. There was no increase in the urinary cyclopropanecarboxylic acid excretion when cypermethrin was administered as a repeated oral dose. Subjects excreted, on average, 72% of the trans isomer dose and 45% of the cis isomer dose respectively in the subsequent 24 h periods after dosing. 4. Approximately 0.1% of the applied dermal dose of 25 mg cypermethrin was excreted within 72 h as the urinary cyclopropanecarboxylic acid. No conclusions can be drawn from such urinary excretion data as to the concentration of cypermethrin and its metabolites in the skin or other organs, or the possibility of other routes of metabolism or excretion.

Chromatography, Gas↗
PubMed1989

Sex differences in the metabolism and excretion of nilvadipine, a new dihydropyridine calcium antagonist, in rats.

1. The metabolic profiles of nilvadipine in the urine and bile of male and female rats were studied after i.v. dosing with 1 mg/kg of the 14C-labelled compound. 2. Excretion rates of the dosed radioactivity in male and female rats, respectively, in the first 48 h were 84.1% and 59.1% in bile, 12.0% and 36.9% in urine, and 2.5% and 3.6% in faeces. 3. Comparison of biliary and urinary excretion for each radioactive metabolite after dosing with 14C-nilvadipine, showed marked sex-related differences in the excretion routes of several metabolites. In male rats, metabolite M3, having a free 3-carboxyl group on the pyridine ring, was not excreted in urine, but in female rats urinary excretion of M3 accounted for 4.7% of the dose. One reason for the lower urinary excretion of radioactivity by males than by females was that the main metabolite, M3, was not excreted in the urine of the male rats. 4. To clarify the sex difference in the route of excretion of M3, this metabolite (M3) was given i.v. to rats. No excretion of the metabolite was observed in urine of male rats within 24 h but, in marked contrast, 41.5% of the dose was excreted in urine of females in the same period.

Animals↗