Urinary prostaglandin and kallikrein excretion are not flow dependent in the rat

To study the relationship between urine flow, urinary prostaglandin (PG) and kallikrein excretion in the rat high urine flow was induced in hydropenic Long-Evans rats by either hypotonic volume expansion or with manniitol or with furosemide. PGE, excretion remained unchanged during hypotonic volume expansion (134.5 ± 29.7 before and 153.0 ± 48.9 pg/min after) while it decreased significantly with mannitol (from 166.3 ± 32.4 to 45.2 ± 8.2 pg/min, p<0.01) and with furosemide (from 170.0 ± 20.4 to 29.5 ± 5.3 pg/min, p<0.001). PGF_2α excretion rates were slightly reduced following all three interventions. Urinary kallikrein excretion remained unchanged in all three groups of animals. It is concluded that, in contrast to human and dogs in the rat urine flow and urinary PG excretion are not interlinked.     

Characterization of biological properties of synthetic and biological leukotriene B3

The effect of micropuncture of the renal papilla through an intact ureter on urinary concetrating ability of rats was examined. Micropuncture of the renal papilla caused a fall in urine osmolality in the punctured kidney from 1718 ± 106 to 1035 ± 79 mosmol/kg·H₂O. In order to investigate the role of renal prostaglandins in this process, PGE₂ excretion was measured and found to increase from 63.4 ± 14.0 to 205.5 ± 57.1 pg/min. Urine osmolality and PGE₂ excretion from the contralateral kidney were not significantly altered. In animals given meclofenamate (2 mg/kg·hr), renal PGE₂ excretion was reduced to 22.3 ± 5.1 pg/min prior to micropuncture and it remained low at 8.9 ± 1.8pg/min after papillary micropuncture. Meclofenamate also blocked the fall in urine osmolality caused by micropuncture of the renal papilla, with urine osmolality averaging 1940 ± 122 before and 1782 ± 96 mosmol/kg·H₂O after the micropuncture. These results indicated that papillary micropuncture through an intact ureter increased renal PGE₂ excretion and that a rise in renal production of PGE₂ or some other prostanoid is associated with a fall in urine concentrating ability.     

Biliary and urinary excretion of peptide leukotrienes in the domestic pig

The metabolism of leukotriene (LT)C₄ and its major routes of elimination have been studied in four anesthetized domestic pigs administered intravenous [³H]-LTC₄ (0.5 μCi/kg). The kinetic profile of LTC₄ in the blood was followed for 60 min after administration while the biliary and urinary excretion of LTC₄ and its metabolites were determined over a 120 min interval. The total recovery of radioactivity in bile and urine was 45% ± 1 (n = 3) and 18% (n = 2) respectively. Examination of the radioactive metabolites in bile showed LTD₄ (44% of biliary content) and LTE₄ (21% of biliary content) as the major identified lipoxygenase products at t (27 min). The only identified cysteinyl leukotriene observed in the urine was LTE₄ (13% of urinary content). In both bile and urine substantial amount of radioactivity were detected at the solvent front of the reverse phase chromatographic system indicating the presence of additional unidentified metabolites. We suggest that measurement of metabolites using these sampling methods may be useful for the detection and measurement of peptide leukotriene production .     

Renal metabolism of substance P in the dog.

Substance P is a potent vasodilatory, diuretic, and natriuretic agent. Since subcellular fractions of the kidney rapidly inactivate substance P in vitro, the present study was designed to examine this observation $\text{in}$$\text{vivo}$ in anesthetized dogs. Arterial, renal venous, and urinary levels of immunoreactive substance P were determined by radioimmunoassay and were found to be 117±11, 128±12 and 659±104 pg/ml, respectively. The urinary and fractional excretion of immunoreactive substance P were 122±22 pg/min and 6.6±2.0%, respectively. When substance P was infused intravenously, the arterial and renal venous plasma levels of immunoreactive material increased whereas the urinary levels did not change. Infusions of 50 ng/kg/min of substance P significantly decreased mean arterial pressure, urinary volume, creatinine clearance as well as the urinary excretion, clearance, and fractional excretion of immunoreactive substance P. During intrarenal infusion of ¹²⁵I-(8-Tyr) substance P, high levels of radioactive material were found in the urine and renal venous plasma which failed to migrate on thin layer chromatography with intact ¹²⁵I-(8-Tyr) substance P. Thus under these conditions, intact substance P was not released from the kidney into the urine or renal venous blood, but instead circulating substance P was rapidly and completely metabolized, probably by both vascular and tubular elements of the kidney.     

Chronic Sodium Benzoate Therapy in Children with Inborn Errors of Urea Synthesis: Effect on Carnitine Metabolism and Ammonia Nitrogen Removal

Sodium benzoate (SB) therapy is known to increase ammonia (NH₃) nitrogen elimination via conjugation with glycine and excretion as urinary hippurate. In 16 children with inborn errors of urea synthesis we studied two issues: (1) the effect of chronic SB administration upon carnitine metabolism and (2) the efficacy of chronic SB therapy as measured by the molar ratio of hippurate excretion to SB intake. Measurements were performed during elective hospitalizations when the patients were in stable metabolic condition. We found that chronic SB therapy is not associated with a constant level of hippurate elimination and that interindividual and intraindividual variability may result in irregular removal of NH₃nitrogen. This variability may be due to various factors including the formation of small quantities of benzoylcarnitine, which was detected in the plasma of three of four patients receiving SB and carnitine therapy and in one of two patients on SB therapy without carnitine supplementation. The ratios of acyl to free carnitine were elevated in both plasma and urine in patients not receiving carnitine supplementation, but were normal in patients receiving supplementation.     

Tissue distribution,metabolism, and elimination of perfluorooctanoic acid in male and female rats

The elimination, tissue distribution, and metabolism of [1-¹⁴C]perfluorooctanoic acid (PFOA) was examined in male and female rats for 28 days after a single ip dose (9.4 μmol/kg, 4 mg/kg). A sex difference in urinary elimination of PFOA-derived ¹⁴C was observed. Female rats eliminated PFOA-derived radioactivity rapidly in the urine with 91% of the dose being excreted in the first 24 hr. In the same period, male rats eliminated only 6% of the administered ¹⁴C in the urine. The sex-related difference in urinary elimination resulted in the observed difference in the whole-body elimination half-life (t_1/2) of PFOA in males (t_1/2 = 15 days) and females (t_1/2 < 1 day). Analysis of PFOA-derived ¹⁴C in tissues showed that the liver and plasma of male rats and the liver, plasma, and kidney of female rats were the primary tissues of distribution. The relatively high concentration of PFOA in the male liver was further examined using an in situ nonrecirculating liver perfusion technique. It was shown that 11% of the PFOA infused was extracted by the liver in a single pass. The ability of the liver to eliminate PFOA into bile was examined in rats whose renal pedicles were ligated to alleviate sex differences in the urinary excretion of PFOA. In a 6-hr period following IP administration of PFOA, there was no apparent difference in biliary excretion, where both males and females eliminated less than 1% of the PFOA dose via this route. We hypothesized that the sex difference in the persistence of PFOA was due to a more rapid formation of a PFOA-containing lipid (i.e., a PFOA-containing mono-, di-, or triacylglycerol, cholesteryl ester, methyl ester, or phospholipid) in the male rat. Also, the increased urinary elimination of PFOA in females may have been due to increased metabolism to a PFOA-glucuronide or sulfate ester. However, no evidence that PFOA is conjugated to form a persistent hybrid lipid was obtained, nor were polar metabolites of PFOA in urine or bile detected. In addition, daily urinary excretion of fluoride in male and female rats before or after PFOA treatment were similar, suggesting that the parent compound is not defluorinated. Thus, the more rapid elimination of PFOA from female rats is not due to formation of a PFOA metabolite.     

Production of urine free dopamine from DOPA; A micropuncture study

The contribution of free L-DOPA to urinary dopamine (D) was examined by microinjecting ³H-DOPA into either proximal tubules or the peritubular space of innervated and denervated rat kidneys. Recirculation of radioactive material was corrected for by comparison with excretion of ¹⁴C inulin included in the injectate. Urine radioactivity was characterized by HPLC. 69.4 ± 2.9% of ³H-DOPA microinjected into proximal tubules appeard in urine from the ipsilateral kidney, 14.6 ± 1.6% of the ³H was recovered as D. After microinjection into the subcapsular peritubular space 4 times as much ³H appeared in the urine from the ipsilateral as from the contralateral kidney. Tubular secretion of total ³H and ³HD was calculated by comparison with ¹⁴C inulin excretion. Chronically denervated kidneys secreted 36.0 ± 4.2% of the microinjected ³H; innervated kidneys secreted 35.0 ± 3.0%. ³H-D secretion was 14.5 ± 3.7% and 15.3 ± 2.8% of the total ³H-DOPA microinjected into denervated and innervated kidneys respectively. We estimated that 30% of the urinary free D is derived from circulating free L-DOPA.     

High-performance liquid chromatographic analysis of phenobarbital and phenobarbital metabolites in human urine

A HPLC assay using UV detection and post-column alkalinization was developed to quantify possible urinary excretion products of phenobarbital in human urine. After filtration the urine was injected directly onto the HPLC column for analysis of phenobarbital, p-hydroxyphenobarbital, phenobarbital N-glucosides and phenobarbital N-glucuronides. The accuracy and precision of the assay were within ± 15% and the limit of detection (LOD) was 1 μM, suitable for pharmacokinetic studies. Phenobarbital was administered orally to five male subjects and urine was collected for a period of 96–108 h. Phenobarbital, p-hydroxyphenobarbital, and phenobarbital N-glucosides were detected and quantified in the urine of all five subjects. The phenobarbital N-glucuronides were not detected in the urine. This assay provides a rapid method with improved selectivity to analyze urine for phenobarbital and its metabolites.     

Changes in Renal Function and Oxidative Status Associated with the Hypotensive Effects of Oleanolic Acid and Related Synthetic Derivatives in Experimental Animals

Purpose

The triterpene oleanolic acid (OA) is known to possess antihypertensive actions. In the present study we to compared the effects of the triterpene on mean arterial blood pressure (MAP) and kidney function following acute administration in normotensive animals with those of its related oleanane synthetic derivatives (brominated oleanolic acid, Br-OA and oleanolic acid methyl ester, Me-OA). We also used experimental models of hypertension to further explore the effects of sub-chronic oral OA treatment and evaluated influences on oxidative status.

Methods

OA was extracted from dried flower buds of Syzygium aromaticum using a previously validated protocol in our laboratory. Me-OA and Br-OA were synthesized according to a method described. Rats were supplemented with lithium chloride (12 mmol L^-1) prior to experimentation in order to raise plasma lithium to allow measurements of lithium clearance and fractional excretion (FE_Li) as indices of proximal tubular Na⁺ handling. Anaesthetized animals were continuously infused via the right jugular with 0.077M NaCl. MAP was measured via a cannula inserted in the carotid artery, and urine was collected through a cannula inserted in the bladder. After a 3.5 h equilibration, MAP, urine flow, electrolyte excretion rates were determined for 4 h of 1 h control, 1.5 h treatment and 1.5 h recovery periods. OA, Me-OA and Br-OA were added to the infusate during the treatment period. We evaluated sub-chronic effects on MAP and kidney function in normotensive Wistar rats and in two animal models of hypertension, spontaneously hypertensive rats (SHR) and Dahl salt-sensitive (DSS) rats, during 9-week administration of OA (p.o.). Tissue oxidative status was examined in these animals at the end of the study. Increasing evidence suggests that and renal function disturbances and oxidative stress play major roles in the pathogenesis of hypertension.

Results

Acute infusion OA and oleanane derivatives displayed qualitatively similar effects in decreasing MAP and increasing urinary Na⁺ outputs. The drugs increased the FE_Na and FE_Li without influencing GFR indicating that at least part of the overall natriuretic effect involved proximal tubular Na⁺ reabsorption. Sub-chronic OA administration (p.o.) also elicited hypotensive responses in Wistar, DSS and SHR rats. The MAP lowering effect was more marked in hypertensive animals and were positively correlated with increased urinary Na⁺ excretion. Compared with respective control rats, OA treatment reduced malondialdehyde (MDA, a marker of lipid peroxidation) and increased activities of antioxidant enzymes; superoxide dismutase and glutathione peroxidase in hepatic, cardiac and renal tissues.

Conclusions

OA and oleanane derivatives have similar effects on MAP, kidney function and oxidative stress. The amelioration of oxidative stress and blood pressure lowering effects by OA are more marked in hypertensive animals and correlated with an increased urinary Na⁺ output.

Novelty of the Work

The results of this study are novel in that they show 1) a correlation between blood pressure reduction and increased urinary Na⁺ excretion by OA, 2) a more marked MAP reduction in hypertensive animals and 3) a drug-induced decrease in proximal tubule Na⁺ reabsorption. The results may also be clinically relevant because OA is effective via oral administration.     

Exacerbation of Underlying Hypothyroidism Caused by Proteinuria and Induction of Urinary Thyroxine Loss: Case Report and Subsequent Investigation

ObjectiveTo describe a patient with excess urinary thyroxine (T₄) excretion and worsening of preexisting hypothyroidism in the setting of nephrotic syndrome and to determine whether excess urinary T₄ excretion is present in other patients with proteinuria.MethodsWe present data regarding the patient’s initial presentation, diagnostic studies, and course of her illness. We suspected urinary T₄ loss to be the cause of her presentation and analyzed her urine sample for total T₄. We also analyzed differences in urinary T₄ excretion in 22 patients with proteinuria and 16 control patients without proteinuria. Relevant medical literature is reviewed.ResultsA 44-year-old woman presented with a 3-month history of increasing fluid retention, weight gain, and fatigue. She had long-standing hypothyroidism on a stable levothyroxine dosage, 125 mcg/d. She had gained 27 kg and had developed significant edema. She had a grossly elevated thyroid-stimulating hormone level of 91 mIU/L. Her condition worsened, and a urinary protein measurement was 14.06 g/24 h—diagnostic of nephrotic syndrome. The levothyroxine dosage was increased to 225 mcg/d. Urinary total T₄ concentration in a 24-hour sample was 59.0 μg/L (83.1 μg/24 h), indicating that a substantial fraction of her orally ingested T₄ was lost in urine. Urinary total T₄ excretion was significantly higher in patients with proteinuria (mean ± standard deviation, 18.0 ± 18.2 μg/L) vs control patients without proteinuria (mean, 3.8 ± 1.8 μg/L) (P = .0014).ConclusionIn the patient described, urinary T₄ loss due to proteinuria and nephrotic syndrome resulted in a severe exacerbation of underlying hypothyroidism. (Endocr Pract. 2008;14:97-103)     

Norepinephrine Metabolism in Humans Studied by Deuterium Labelling: Turnover of 4–Hydroxy-3–methoxyphenylglycol

Abstract: D, L(±)-4-Hydroxy-3-methoxyphenylglycol (HMPG) labelled with three deuterium atoms was used to study turnover of plasma free HMPG following an intravenous injection. Ten healthy men were given a pulse dose of either 4.3 μmol or 2.2 μmol of labelled HMPG ([²H₃]HMPG piperazine salt). Plasma and urine levels of both endogenous and labelled HMPG were subsequently followed by gas chromatography-mass spectrometry with selected ion detection. Kinetic calculations based upon a single-compartment model were consistent with a monoexponential elimination of plasma free HMPG. The half-life of HMPG was 0.46 and 0.78 h (mean values in the two dose groups). The HMPG production rate was 2.01 and 2.35 μmol/hour, and the urinary excretion rate of HMPG (free and conjugated) was 0.48 and 0.47 μmol/h. The endogenous plasma level of free HMPG was 25 and 33 nmol/L. The results show that HMPG turns over rapidly and that HMPG is further metabolized extensively. About one-fourth of the HMPG produced is excreted in urine as free and conjugated HMPG.     

The Effect of Various Carbonate Sources on the Survival of Escherichia coli in Dairy Cattle Manure

Manure slurries (n = 3) prepared from the feces and urine of lactating dairy cattle (1 part urine, 2.2 parts feces, and 6.8 parts distilled water) had an initial pH of 8.6 ± 0.1; dissolved carbonate concentrations of 48 ± 4 mm, and Escherichia coli counts of 5.9 ± 0.7 logs per ml slurry. The pH of untreated slurries declined to pH 7.0 ± 0.1 by the 10th day of incubation, and the E. coli count increased approximately 10-fold (P < 0.05). When slurries were treated with Na₂CO₃, K₂CO₃, NaHCO₃ or Na₂CO₃·NaHCO₃ (0 to 16 g/kg slurry), the dissolved carbonates increased in a linear fashion, but only Na₂CO₃ and K₂CO₃ (8 g/kg or greater) or Na₂CO₃·NaHCO₃ (16 g/kg) ensured an alkaline pH. Even relatively low concentrations of Na₂CO₃ or K₂CO₃ (8 or 12 g/kg) caused a decrease in E. coli viability (P < 0.05), and E. coli could not be detected if 16 g/kg was added (day 5 or 10 of incubation). Na₂CO₃·NaHCO₃ also caused a decrease in E. coli viability, (P < 0.05), but some E. coli (approximately 10⁴ cells per g) were detected on day 10 even if the concentration was 16 g/kg. NaHCO₃ did not prevent the decrease in pH or cause a decrease in E. coli numbers (P > 0.05). Calculations based on the Henderson-Hasselbalch equation (pH and dissolved carbonates) indicated that little E. coli killing was noted until the dissolved carbonate anion concentrations (CO₃ ⁻²) were greater than 1 mm, but bicarbonate anion (HCO₃ ⁻) concentrations as high as 180 mm did not affect E. coli viability. These results are consistent with the idea that carbonate anion has antimicrobial properties and can kill E. coli in dairy cattle manure. Received: 20 December 2000 / Accepted: 7 February 2001     

Biliary, fecal and uninary excretion of [H]-prostaglandins in the rat

The profiles of biliary, fecal and urinary excretion of tritium labeled prostaglandins (PG's) of differing biological activity were investigated in the rat. The PG's (10 μg/kg: 2 to 50 μCi/rat, in 1 ml polyethylene glycol-400) were administered intragastrically. Excretion data were expressed as a percentage of the total administered radioactivity. for the orally administered PG's 11R-methyl-16R-fluoro-15R-hydroxy-9-oxoprosta- -5- -13-dienoic acid and its methyl ester, excretion was equally divided between urine and feces. The fecal and urinary profile of excretion of ³H after prostacyclin (PGl₂) was similar to that following administration of 11R, 16, 16-trimethyl-15R-hydroxy-9-oxoprosta- -5- -13-dienoic acid (trimoprostil), a PG with antisecretory-antiulcer potential. However, PGl₂ was very poorly absorbed from the intestine, while the absorption of trimoprostil was very efficient. Biliary excretion, with little entero-porto-hepatic biliary circulation, was the main route of elimination of trimoprostil, thereby resulting in rapid elimination of drug-related products and diminishing the potential for systemic liability in the rat.     

Regulation of urinary thromboxane B2 in man: Influence of urinary flow rate and tubular transport

Thromboxane B₂ (TxB) is excreted in human urine, but the mechanism of renal excretion and the quantitative relationship of urinary TxB to the active parent compound, thromboxane A₂, of renal or extrarenal origin is not established. To determine the effects of vasoactive hormones, uricosuric agents and urinary flow rate on TxB excretion, urinary TxB was measured by radioimmunoassay and mass spectrometry, and renal metabolism of blood TxB was determined by radiochromatography of urine after i.v. [³H]-TxB infusions. Basal TxB was 6.7 ± 1.1 ng/h during an oral water load, and TxB fell with s.q. antidiuretic hormone (to 3.4 ± 0.4 ng/h, P<0.01) and with fluid restriction (to 2.6 ± 0.5 ng/hr, P=0.001) in parallel with urinary volume. Urinary excretion of unmetabolized [³H]-TxB also fell (by 56%) with fluid restriction, implicating altered metabolism rather than synthesis as the mechanism of the urinary flow effect. Angiotensin II infusions slightly reduced both TxB and urine volume, consistent with a flow effect. In contrast, probenecid did not alter urine volume, but increased urinary uric acid (by 244%), TxB (from 5.6 ± 0.9 to 11.1 ± 2.9 ng/h) and urinary excretion of blood [³H]-TxB (by 243%) by similar amounts (all P<0.05), suggesting that TxB is actively reabsorbed in the proximal tubule, similarly to uric acid. Thus, urinary excretion of TxB of renal and extrarenal origin is regulated by proximal and distal tubule factors.     

Renal excretion of perfluorooctanoic acid in male rats: Inhibitory effect of testosterone

There is a marked sex difference in the whole-body elimination of perfluorooctanoic acid (PFOA) in rats, with females excreting the perfluorinated acid much more rapidly (half life [t_1/2] < 1 day) than males (t_1/2=15 days). Our objective was to determine if androgens or estrogens are involved in causing this sex difference in PFOA elimination. Castration of males greatly increased the elimination of [1-¹⁴C]PFOA (9.4 μmiol/kg, i.p.) in urine, demonstrating that a factor produced by the testis was responsible for the slow elimination of PFOA in male rats. Castration plus 17β-estradiol had no further effect on PFOA elimination whereas castration plus testosterone replacement at the physiologic level reduced PFOA elimination to the same level as rats with intact testes. Thus, in male rats, testosterone exerts an inhibitory effect on renal excretion of PFOA. In female rats, neither ovariectomy nor ovariectomy plus testosterone affected the PFOA urinary elimination, demonstrating that the inhibitory effect of testosterone on PFOA renal excretion is a male-specific response. Probenecid decreased the high rate of PFOA renal excretion in castrated males but had no effect on male rats with intact testes. We conclude that testosterone is a key determinant of the sex difference in PFOA elimination in rats.     

Method for measuring endogenous 3-O-methyldopa in urine and plasma

The present report describes a method using column liquid chromatography with electrochemical detection for assaying concentrations of 3-O-methyldopa in urine and plasma. The technique combines a one-step sample preparation scheme with post-column flow-through electrodes in series, allowing adequate chromatographic separation of 3-O-methyldopa from other endogenous substances in urine. The validity of the method was confirmed by markedly decreased urinary 3-O-methyldopa levels after administration of an inhibitor of catechol-O-methyltransferase to rats, radioactivity in chromatographic fractions corresponding to 3-O-methyldopa in urine of rats undergoing infusion of [³H]-l-DOPA, and correlations between excretion rates of 3-O-methyldopa and catechols in humans. In healthy humans, urinary excretion of 3-O-methyldopa averaged 974 ± 707 (S.D.) nmol per day, and plasma levels of 3-O-methyldopa averaged 89 ± 32 nmol/l. The method should be useful in studies about the metabolism of endogenous and exogenous DOPA.     

Stimulation of ammonium ion excretion in the toad urinary bladder by an extract of human urine

It is well known that ammonium ion excretion is increased during metabolic acidosis in mammals. The purpose of this study was to determine whether we could isolate from human urine during metabolic acidosis a factor that would stimulate NH₄⁺ and/or H⁺ excretion in toad urinary bladder. Extracts of urine from six human subjects collected during NH₄Cl-induced acidosis were prepared. These extracts were tested for their effect on NH₄⁺ excretion in hemibladders mounted between plastic chambers. The extracts significantly increased NH₄⁺ excretion in the toad urinary bladder. We found no effect on H⁺ excretion by these extracts. This ammoniuretic activity was not present in the urine when the same individuals were in metabolic alkalosis. We conclude that during metabolic acidosis a humoral factor is present which stimulates the excretion of NH₄⁺. The factor could act as a permease in the bladder cell or as a stimulator of an NH₄⁺ transport system.     

Digestibility and utilisation of diets composed of wet distillers' solids or soyabean meal and supplemented with liquid lysine product for growing pigs

A digestibility and balance trial was carried out to study the nutrient digestibility and utilisation of protein and energy in wet distillers' solids derived from barley or soyabean meal. Eight growing pigs (30–72 kg liveweight) were used in an 8 × 6 cyclic change-over experimental design, in which eight experimental diets were arranged 2 × 2 × 2 factorially. The corresponding factors were the protein source (wet distillers' solids (DS) or soyabean meal (SBM)), protein supply (130 or 162 g crude protein (CP) kg⁻¹ dry matter (DM)) and liquid lysine product supplementation.DS and SBM contained 565 g and 485 g CP kg⁻¹ DM, respectively, and the respective lysine contents in CP were 39 g and 64 g per 160 g N. The liquid lysine product contained 527 g CP kg⁻¹ DM and lysine in CP 193 g per 160 g N.No differences were found in the total tract digestibility of the nutrients or energy among diets composed of DS or SBM without lysine supplementation. Those diets with liquid lysine product supplementation, however, had opposite effects on the digestibility of the diets composed of the different protein sources. Lysine supplementation improved the digestibility of ash (P < 0.001), ether extract (P < 0.05) and crude carbohydrates (CCH) (P < 0.05) in diets composed of DS and adversely impaired the digestibility of organic matter and CCH (P < 0.05) in diets composed of SBM. The calculated digestibility of CP and gross energy were respectively 91.2% and 88.3% in SBM and 90.2% and 85.0% in DS. The digestible and calculated net energy contents were respectively 18.16 MJ kg⁻¹ DM and 10.73 MJ kg⁻¹ DM for SBM and 19.31 MJ kg⁻¹ DM and 10.40 MJ kg⁻¹ DM for DS.The pigs on the diets composed of DS had higher total (P < 0.001) and urea (P < 0.01) nitrogen (N) excretion in urine and lower daily retention of N (P < 0.001) than the pigs on the diets composed of SBM. The liquid lysine product supplementation of the diets decreased the total and urea N excretion in urine (P < 0.001) and improved the daily N retention (P < 0.001). With lysine supplementation, the protein utilisation of the diets composed of DS was improved to the level of the diets composed of SBM. No differences were observed in the utilisation of energy among the diets composed of different protein sources.It is concluded that DS is highly digestible, but its protein is efficiently utilised only with lysine supplementation.     

Human biokinetics of strontium—part II: Final data evaluation of intestinal absorption and urinary excretion of strontium in human subjects after stable tracer administration

Fractional intestinal absorption (f ₁ value) and urinary excretion of strontium in healthy human volunteers has been measured by simultaneous oral and intravenous administration of the stable isotopes ⁸⁶Sr and ⁸⁴Sr using the double-isotope method. Final evaluation of the complete data set confirmed that ingestion of different foodstuff and nutritional factors could influence the fractional gut uptake of strontium. In some cases, significant deviations from the f ₁ value adopted by the International Commission on Radiological Protection (ICRP) were found. The arithmetic mean (± standard deviation) of the f ₁ values of all experiments performed was determined to be 0.46 (± 0.24). The probability distribution function of the f ₁ values is represented by a lognormal curve with a geometric mean of 0.38 and a geometric standard deviation of 2.06. Urinary excretion in all subjects varied depending on the administered foodstuff in a wide range and differs from the ICRP model, up to 2 days after tracer administration. No age or gender dependence of the absorbed strontium fraction and of the urinary excretion of strontium after an oral load was found.     

Quantitative analysis of two dinor urinary metabolites of prostaglandin I2

The synthesis of deuterium- and tritium-labeled analogs of 2,3-dinor-6-keto-prostaglandin F_1α and of 6,15-diketo-13,14-dihydro-2,3-dinor-prostaglandin F_1α is described. These analogs were used as internal standards in the assay of the corresponding unlabeled metabolites in human urine by stable isotope dilution and combined gas chromatography-mass spectrometry. In male subjects the 24-h urinary excretion of the two metabolites was found to be 719 ± 264 and 314 ± 115 ng, respectively. The method offers a noninvasive approach to the study of prostaglandin I₂ synthesis in man.