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PubMed2005

Effects of intra-peritoneal injection with NH4Cl, urea, or NH4Cl+urea on nitrogen excretion and metabolism in the African lungfish Protopterus dolloi.

This study aimed to (1) determine if ammonia (as NH(4)Cl) injected intra-peritoneally into the ureogenic slender African lungfish, Protopterus dolloi, was excreted directly rather than being converted to urea; (2) examine if injected urea was retained in this lungfish, leading to decreases in liver arginine and brain tryptophan levels, as observed during aestivation on land; and (3) elucidate if increase in internal ammonia level would affect urea excretion, when ammonia and urea are injected simultaneously into the fish. Despite being ureogenic, P. dolloi rapidly excreted the excess ammonia as ammonia within the subsequent 12 h after NH(4)Cl was injected into its peritoneal cavity. Injected ammonia was not detoxified into urea through the ornithine-urea cycle, probably because it is energetically intensive to synthesize urea and because food was withheld before and during the experiment. In addition, injected ammonia was likely to stay in extracellular compartments available for direct excretion. At hour 24, only a small amount of ammonia accumulated in the muscle of these fish. In contrast, when urea was injected intra-peritoneally into P. dolloi, only a small percentage (34%) of it was excreted during the subsequent 24-h period. A significant increase in the rate of urea excretion was observed only after 16 h. At hour 24, significant quantities of urea were retained in various tissues of P. dolloi. Injection with urea led to an apparent reduction in endogenous ammonia production, a significant decrease in the hepatic arginine content, and a significantly lower level of brain tryptophan in this lungfish. All three phenomena had been observed previously in aestivating P. dolloi. Hence, it is logical to deduce that urea synthesis and accumulation could be one of the essential factors in initiating and perpetuating aestivation in this lungfish. Through the injection of NH(4)Cl + urea, it was demonstrated that an increase in urea excretion occurred in P. dolloi within the first 12 h post-injection, which was much earlier than that of fish injected with urea alone. These results suggest that urea excretion in P. dolloi is likely to be regulated by the level of internal ammonia in its body.

Amino Acids↗
PubMed1987

Virus excretion and strain specific antibody responses after oral poliovaccine in previously immunised children.

A nation-wide campaign with trivalent oral poliovirus vaccine was organized in Finland in February-March 1985 in order to stop the unexpected outbreak of poliomyelitis. Excretion time of the vaccine viruses and antibody responses due to vaccination were studied in a group of healthy 6-year-old children who were classmates to one of the patients during the outbreak and who also had been screened for excretion of the epidemic poliovirus type 3 strain. While faecal excretion of at least one of the three vaccine virus serotypes was documented in all 19 children, only one throat specimen out of 106 studied was positive in the virus isolation test. The mean excretion times for types 1, 2, and 3 were 13, 21, and 21 days, respectively, and five children were still excreting a vaccine virus strain at 5 wk. Faecal excretion of the type 3 vaccine virus was not seen in children who had been excreting the epidemic type 3 strain 4 mo earlier. Excretion of a respective vaccine virus strain was usually well correlated to a booster response in serum neutralising antibodies to types 2 and 3 but not to type 1 poliovirus. A relatively high prevaccination antibody level did not always prevent the take of the corresponding vaccine virus strain. An increase in the level of neutralising serum antibodies towards at least one poliovirus serotype was observed in all but one of the 17 children studied. Antibody responses to the live vaccine strains were similar to those towards the corresponding nonattenuated strains while the absolute antibody titres against the epidemic P3/Finland/23127/84 strain remained relatively low in most sera studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Glutamate excretion as a major kinetic bottleneck for the thermally triggered production of glutamic acid by Corynebacterium glutamicum.

The study was aimed at evaluating the extent of flux control exercised by the amino acid excretion step on the glutamate production flux in C. glutamicum 2262 strain that is induced for glutamate excretion by an upward temperature shift. Cells initially induced to excrete glutamate were cultivated at different controlled temperatures between 33 and 40 degrees C, and changes in glutamate excretion flux and intracellular concentration were determined in response to increased culture temperature. The fastest growth rate of 0.45 h(-1) and the lowest glutamate excretion rate of 1 mmole/g dw x h were observed at 33 degrees C, together with a high intracellular 0.5 mmole/g dw glutamate accumulation. On the contrary, the fastest glutamate excretion rate of 6 mmole/g dw x h was obtained at 40 degrees C, when cell growth was arrested and the internal glutamate level reduced to 0.25 mmol/g dw. The observed sixfold increase in excretion flux as a result of the temperature increase clearly suggests a specific effect of temperature on the glutamate export system which appears as the major kinetic bottleneck for the glutamate production flux. This conclusion is corroborated by the high internal accumulation of glutamate which, even under the fastest excretion conditions, severely inhibits the activity of the glutamate biosynthesis pathway.

Bioreactors↗
PubMed2001

Increased biliary excretion of thyroxine by microsomal enzyme inducers.

The extrathyroidal mechanism by which endocrine disruptors promote thyroid tumors has been proposed to be increased glucuronidation and biliary elimination of thyroxine (T(4)), followed by disruption of the hypothalamic-pituitary-thyroid axis. The ability of a chemical to increase T(4) glucuronidation in vitro correlates with the ability to reduce serum T(4) concentrations. Pregnenolone-16alpha-carbonitrile (PCN), 3-methylchloranthrene (3-MC), and Aroclor 1254 (PCB) each increase T(4) glucuronidation in rat liver microsomes and reduce serum T(4). However, whether reductions in serum T(4) result directly from increases in T(4) glucuronidation and biliary excretion in vivo has not been thoroughly examined. It is also unclear whether reduced serum T(4) concentrations following microsomal enzyme inducer treatment elicit increases in serum thyrotropin (TSH), the primary stimulus for thyroid cell proliferation, because only PCN treatment increases serum TSH. This study sought to determine whether increases in T(4)-glucuronide biliary excretion in vivo are responsible for reductions in serum T(4) and increases in serum TSH. Male rats were fed control diet or diet containing either 1000 ppm PCN, 250 ppm 3-MC, or 100 ppm PCB for 7 days. Animals were then given [(125)I]T(4) iv, and bile was collected for 2 h. Radiolabeled metabolites in bile were analyzed by reverse-phase HPLC with gamma-detection. PCN, 3-MC, and PCB treatments reduced serum T(4) concentrations by 42, 45, and 73%, respectively, while TSH was only increased by PCN (180%). The biliary excretion of [(125)I]thyronines was increased 103% by PCN, 157% by 3-MC, and 193% by PCB. T(4)-glucuronide was the primary metabolite in bile, accounting for up to 86% of the radiolabeled metabolites in controls. The amount of T(4)-glucuronide excreted in bile was increased 161% and 226% by 3-MC and PCB, respectively, but was only increased 55% by PCN. None of the treatments had any effect on the urinary excretion of [(125)I]T(4). Thus, increased glucuronidation and biliary excretion of T(4) appears likely to be responsible for reductions in serum T(4) produced by microsomal enzyme inducers. Furthermore, increases in T(4) biliary excretion produced by microsomal enzyme inducer treatment are not consistent with changes in TSH. Thus, it can be concluded that differential changes in serum TSH do not stem from differential increases in T(4) biliary excretion.

Animals↗
PubMed1986

Urinary kallikrein excretion in healthy young infants.

Nineteen healthy hospitalized children aged between 3 weeks and 10 years and 20 others aged between one month and 16 years have been investigated for their excretion rate of active and total urinary kallikrein. Twelve hour urine samples were obtained between 7 p.m. and 7 a.m. and blood was drawn at the end of the urine collection period. Urinary kallikrein activity was measured by a synthetic substrate and a direct RIA and urinary sodium excretion, urine volume and plasma renin activity (PRA) were determined. Urinary kallikrein activity was found to be between 0 and 6 micrograms/24h and constituted approximately 10-20% of total kallikrein. When urinary kallikrein excretion rate was correlated with the sodium excretion rate the relationship was found to be positive and significant as was the correlation found between urine volume and urinary kallikrein excretion rate. No correlation could be found between PRA and urinary kallikrein excretion. Although a tendency of higher total kallikrein excretion was seen in older children, the amount excreted from all children per kilogram body weight was constant at 0.8 microgram/kg.

Child↗
PubMed1979

Role of purine base excretion in regulation of purine pools.

Wild type and mutant strains of Neurospora crassa excrete hypoxanthine, xanthine, and uric acid, but not adenine or inosine, when exogenous adenine is added to growing cultures. No detectable excretion occurs in the absence of adenine. The de novo pathway of purine biosynthesis was found to influence the excretion, in that a metabolic block immediately prior to IMP significantly decreased the excretion, while a metabolic block immediately after IMP significantly increased the excretion over that of wild type. The purine catabolic pathway, which is sensitive to ammonia regulation, was found to be a key determinant in the amount and type of excretion. Recently, it was suggested that hypoxanthine accumulation is the result of a mechanism to regulate the adenylate pool size (Leung and Schramm, 1978). In this report, the possibility that hypoxanthine excretion controls adenylate and guanylate pool sizes is discussed and the role of the purine nucleotide cycle in hypoxanthine excretion is examined.

Adenine↗
PubMed1995

Albumin excretion rate levels in non-diabetic offspring of NIDDM patients with and without nephropathy.

Familial clustering of diabetic nephropathy points to genetic susceptibility. The observation that in non-diabetic subjects microalbuminuria occurs more frequently in the presence of a parental history of diabetes supports this hypothesis. However, the role of inherited factors in poorly understood in non-insulin dependent diabetes mellitus (NIDDM). This study investigated the albumin excretion rate in non-diabetic offspring of NIDDM patients with increased albumin excretion rate (> 20 micrograms/min) or normal albumin excretion rate (< 20 micrograms/min). We recruited 20 offspring of NIDDM patients with increased albumin excretion rate (A-off) and 20 offspring rate (N-off), matched for age, sex, body mass index, blood pressure and estimated protein intake. All offspring were normotensive, had normal creatinine clearance, normal glucose tolerance and sterile urine collection. Albumin excretion rate was measured on three sterile overnight urine collections and median values were used for calculations. Albumin excretion rate was significantly higher in A-off than in N-off (7.7 +/- 1.2 vs 3.4 +/- 0.6 micrograms/min p<0.01) and significantly related to parents' albumin excretion rate (p<0.01, r=0.53). These results suggest that an increased glomerular permeability is present in non-diabetic offspring of NIDDM patients with increased albumin excretion rate.

Adult↗
PubMed1979

3-Methoxy-4-hydroxyphenylglycol excretion in acutely schizophrenic patients during a controlled clinical trial of the isomers of flupenthixol.

Urinary MHPG excretion in patients with acute schizophrenia was studied before and during a trial of the isomers of flupenthixol and placebo. Pretrial MHPG excretion was not related to severity of illness before the trial or to other pretrial clinical variables. In male subjects higher pretrial MHPG excretion was associated with a better outcome 1 year post-trial. However in females no relationship between MHPG excretion and outcome was established. During the trial there was a reduction in MHPG excretion in patients treated with beta-flupenthixol but no decrease in the group treated with alpha-flupenthixol or chlorpromazine. In patients on placebo there was a reduction in MHPG excretion in those who did well clinically, but not in those who did poorly. Thus low MHPG excretion may be a predictor of poor outcome in schizophrenia, but MHPG excretion also changes both as a function of clinical state and of neuroleptic drug administration.

Adult↗
PubMed1975

A comparison of sodium excretion in response to infusion of isotonic saline into the vena porta and vena cava of conscious rats.

1. Indwelling non-occlusive catheters were placed in the vena porta and inferior vena cava of female rats several days before experimentation. Isotonic saline or isosmotic glucose (2% of body wt.) was infused into one vein followed one to several days later with an identical infusion into the other vein of each conscious animal. 2. Significantly higher urine flow and sodium excretion resulted from infusion of isotonic saline (0.5 ml/min) into the vena porta than into the vena cava. Modest prehydration or section of the hepatic branch of the right vagus did not affect the differential sodium response. Changes in endogenous creatinine clearance and potassium excretion were not significantly different for the two routes. Mean values for net peak sodium excretion and contemporaneous urine flow, urinary sodium concentration, and fractional sodium excretion were significantly higher for the portal than for the caval infusion while differences in glomerular filtration rate and filtered sodium load were insignificant. No significant difference in sodium excretion resulted from infusion of isosmotic glucose by the two routes. 3. Compared to the response promoted by the isotonic saline load infused at 0.5 ml/min, the differential response in sodium excretion was prolonged when the same load was infused at 0.375 ml/min. Sodium excretion was not significantly different for the two routes when the same isotonic saline load was infused at 0.75 ml/min. 4. These experiments provide evidence for participation of the liver in the control of sodium excretion and suggest release of a hepatic humoral factor which may be controlled by the duration of exposure of the hepatic circulation to an adequate load of isotonic saline.

Animals↗
PubMed1988

Urinary excretion of 6-keto prostaglandin F1 alpha in pre-eclampsia.

In order to investigate whether urinary excretion of prostaglandins (PG) is involved in the pathophysiology of pre-eclampsia, urinary immunoreactive 6-keto PGF1 alpha and TXB2 were measured in normal and pre-eclamptic women by radio-immunoassay after extraction with Bond Elut column. Urinary levels of 6-keto PGF1 alpha and TXB2 were expressed as ratio of urinary concentration of prostaglandin vs. creatinine (pg prostaglandin/mg creatinine; pg/mg cre.). Urinary excretion in normal pregnant and postpartum women were 211.2 +/- 33.8 and 160.1 +/- 9.1 pg/mg cre., respectively. In the pre-eclamptic group, urinary excretion of 6-keto PGF1 alpha was 105.3 +/- 28.2 pg/mg cre. in pregnancy and 99.0 +/- 12.5 pg/mg cre. in the postpartum period. Urinary excretion of 6-keto PGF1 alpha in the pre-eclamptic group was significantly lower (P less than 0.05) than in normal controls during pregnancy but not in the postpartum period. Urinary excretion of TXB2 was not significantly different between the two groups. The urinary excretion of 6-keto PGF1 alpha was measured before and after the onset of pre-eclampsia in four cases of edema and weight gain of more than 500 g/week (group e), one case of proteinuria of more than 200 mg/dl with edema (group ep) and three cases of pre-eclampsia (group eph). The urinary excretion of 6-keto PGF1 alpha in these eight patients before onset of pre-eclampsia was slightly lower than of normal controls but not significantly so. In group eph, urinary excretion of PG was decreased after the onset of pre-eclampsia. These results provide further evidence of the involvement of PG in the pathophysiology of pre-eclampsia.

6-Ketoprostaglandin F1 alpha↗
PubMed1976

[Diurnal variation in the urinary excretion of vanilmandelic acid and aldosterone in normal and hypertensive persons (author's transl)].

The excretion of creatinine, VMA, and aldosterone was measured in the urine of 14 normal and 25 persons with stable essential hypertension during a day time (7.00-23.00 hrs) and a night time (23.00-7.00 hrs) period. Excretion of VMA and aldosterone per hour in the two groups was lower during the night period than during the day. No significant difference existed between the excretion values of both groups. Night/day rations for the excretion of VMA and of aldosterone respectively, per mg of creatinine excreted were calculated for each subject. In the normal group the night/day ratios of aldosterone excretion showed a significant correlation to the corresponding ratios of VMA excretion; such correlation was not found in the hypertensive group. The fact that a correlation was observed in the normal group is compatible with the hypothesis that catecholamines are involved in the regulation of the renin-angiotensin-aldosterone system. Lack of correlation in the group of hypertensive does not as yet allow any conclusions. In two patients with primary hyperaldosteronism, the aldosterone excretion during the night was relatively more elevated than in the day.

Adult↗
PubMed1976

Effects of parathyroid hormone on H+ and NH+4 excretion in toad urinary bladder.

The urinary bladder of Bufo marinus excretes H+ and NH+4, and the H+ excretion is increased after the animal is placed in metabolic acidosis. The present study was done to determine if parathyroid hormone could stimulate the bladder to increase the excretion of H+ and/or NH+4. Parathyroid hormone added to the serosal solution in a final concentration of 10 mug/ml was found to increase H+ excretion by 50 per cent above the control hemibladders, while there was no effect on NH+4 excretion. Parathyroid hormone had no effect on H+ excretion when added to the mucosal solution. We also performed experiments utilizing theophylline and dibutyryl cyclic AMP which mimicked those of the parathyroid hormone experiments. A dose-response analysis was performed and the results indicate that 1 mug/ml of parathyroid hormone was the minimal effective dose. These results suggest that parathyroid hormone can stimulate H+ excretion in the toad urinary bladder and this effect seems to be mediated by cyclic AMP. In addition, it was found that parathyroid hormone has no effect on NH+4 excretion.

Ammonia↗
PubMed1984

Urinary excretion of histamine and some of its metabolites in man: influence of the diet.

Urinary excretions of histamine, N tau-methylhistamine and N tau-methylimidazoleacetic acid have been determined in 10 normal subjects on 3 different diets, containing a very low protein, a low protein and a high protein amount. Foodstuffs which could contain histamine were excluded. The mean excretion of N tau-methylhistamine on the second day of each diet amounted to 0.861 mumol/24 h, 1.051 mumol/24 h and 1.378 mumol/24 h, respectively. The excretions of histamine and N tau-methylimidazoleacetic acid were not affected. In 6 normal persons on a protein low diet, the excretions of histamine, N tau-methylhistamine and N tau-methylimidazoleacetic acid have been determined for 10 days. On the fifth day, to 3 persons 200 mumol of histamine was given orally, the other 3 persons received a high protein diet. The persons receiving histamine showed a strongly enhanced excretion of N tau-methylimidazoleacetic acid, corresponding to 36.1% of the administered histamine, whereas the urinary excretions of histamine and N tau-methylhistamine were only slightly elevated. On the high protein diet, only the excretion of N tau-methylhistamine was slightly elevated. The urinary excretions of histamine in the female subjects sometimes showed unexpectedly high values. Most probably, this phenomenon is attributable to bacterial histamine production in the urogenital tract.

Acetates↗
PubMed1978

Effects of reserpine and propranolol on urinary excretion of histamine and 5-hydroxytryptamine in severe cold exposure in normal and cold-acclimated Guinea-pigs.

The effects of cold-acclimation, reserpine and propranolol were investigated on the survival time, rectal temperature and urinary excretion of histamine and 5-HT in guinea-pigs at -20 degrees C. Both reserpine and propranolol shortened survival time by 3 hours and 1.5 hours respectively, the shortest time being in the cold-acclimated reserpine-treated animals. There was a trend in severe cold exposure to increased excretion of histamine both in the non-acclimated and in cold-acclimated animals. Reserpine did not change the excretion but increased the concentration of histamine from 0.08 to 0.25 microgram/ml. Propranolol proved to be a histamine liberator by increasing the excretion in non-acclimated from 0.10 to 1.40 microgram/h and concentration from 0.10 to 4.52 microgram/ml and in cold-acclimated animals the excretion from 0.20 to 2.85 microgram/h and the concentration from 0.08 to 3.23 microgram/ml. Severe cold increased the excretion of 5-HT in the non-acclimated animals from 0.08 to 0.21 microgram/h and cold acclimation increased this to 0.17 microgram/h. Reserpine diminished the excretion from 0.08 to 0.03 microgram/h in the non-acclimated animals, but propranolol had no effect. The results showed that the excretion of histamine and 5-HT into urine are changed in cold and can be modified with drugs. The application of the findings in proving a cold stress deserves further study.

Acclimatization↗
PubMed1981

Effect of vitamin D deficiency on urinary excretion of connective tissue derivatives (hydroxyproline and glycosaminoglycans) in rats.

The urinary excretion of two connective tissue metabolites was studied in both control and vitamin D deficient rats. Hydroxyproline (HyPRO) excretion was determined after 2, 13 and 22 months (experiment I). It decreased with aging in animals receiving the control diet. On the contrary, this excretion increased as a function of age in vitamin D deficient animals. At the age of 22 months, HyPRO excretion was respectively 31 and 1708 micrograms a day in control and deficient animals. HyPRO and glycosaminoglycans (GAG) excretion was measured on a group of both control and vitamin D deficient rats at the age of 21 months (experiment II). These results confirm the high excretion of HyPRO in deficient animals. On the contrary, the GAG excretion was higher in control animals than in deficient ones, the mean excretion being respectively 412 and 234 micrograms a day.

Animals↗
PubMed2000

Urinary albumin excretion and transcapillary escape rate of albumin in malignancies.

Transcapillary escape rate of albumin was determined in 22 patients with different malignancies. In addition, urinary albumin excretion rate was measured in 24-h urine samples using a sensitive immunoassay. Increased urinary albumin excretion was defined as >/=20 microg/min according to conventional standards. Renal glomerular filtration and tubular function was estimated by 51Cr-EDTA plasma clearance and urinary beta 2-microglobulin, respectively. Median urinary albumin excretion rate was 15.0 microg/min (range 6-510 microg/min) and the frequency of increased urinary albumin excretion was 41%. This agrees with other studies showing increased albuminuria in several types of malignant diseases. Patients with advanced disease (tumour, node, metastasis (TNM) stage II-IV) had a significantly higher urinary albumin excretion rate than patients with localized disease (TNM stage I). Serum creatinine, glomerular filtration rate and urinary beta 2-microglobulin were all within normal limits. Median transcapillary escape rate of albumin was 5.5 %/h (range 2-8 %/h) and this level is comparable with values in healthy subjects. There was no significant difference in transcapillary escape rate between patients with elevated urinary albumin excretion and the normoalbuminuric group. Median value of the absolut outflux of albumin was 10.6 g/h with similar levels in patients with increased urinary albumin excretion and patients with normoalbuminuria. Our results indicate a high prevalence of minor glomerular dysfunction with a slightly elevated urinary albumin excretion in patients with malignancies. The normal endothelial function, as estimated by the transcapillary escape rate of albumin, suggests an overall unaffected capillary permeability and increased urinary albumin loss appears to be an isolated renal phenomenon in cancer patients.

Adult↗
PubMedDate not supplied

Urinary excretion kinetics of intact quinidine and 3-OH-quinidine after oral administration of a single oral dose of quinidine gluconate in the fasting and non-fasting state.

To obtain more precise urinary excretion data of intact quinidine (D) and its main metabolite, 3-OH-quinidine (DM), the specific HPLC method of Bonora et al has been used to follow its urinary excretion kinetics. In a cross-over study, 2 commercial dosage forms of quinidine gluconate, fast- and slow-release, were administered to 18 healthy subjects who had fasted for 10 hours in 3 treatments which were administered during the fasting period (T1), and before (T2) of after (T3) a standard breakfast. The urine was collected at fixed time intervals for 72 hours after the administration of a single dose (405 mg of quinidine base). The difference between the drug release characteristics of the two products was studied by analysing the cumulative amount of D and DM excreted as a function of time, and the time required to reach the maximum value for the urinary excretion rate of intact quinidine. A food effect could be noticed among treatments with the conventional fast-release dosage form when comparing the maximum values of the urinary excretion rate of D (T2 greater than T1). There was no significant difference in the percentage of drug absorbed from the 2 products, according to the data on the cumulative amount of D and DM. The parameters estimated for quinidine and the metabolite were: the apparent half-life of elimination, the urinary excretion rates and the time to reach a maximum value in the urinary excretion rate. The urinary excretion rate constant and the renal clearance were also quantified for quinidine by combining urinary parameters with the corresponding serum data previously reported.

Administration, Oral↗
PubMedDate not supplied

Absorption, distribution and excretion of 3H-labeled cephaeline- and emetine-spiked ipecac syrup in rats.

The maximum plasma radioactivity levels of tritium (3H)-labeled cephaeline, (24.3, 28.7 and 40.6 ng eq./mL) were reached at 2.00-3.33 hours following oral dosing of ipecac syrup. The maximum plasma radioactivity levels of 3H-emetine (2.71, 6.47 and 9.62 ng eq./mL) were reached at 1.08-2.33 hours following ipecac syrup administration. The Cmax values of 3H-cephaeline were followed by a biexponential decrease with half-lives t 1/2(lambda z) of 3.45-9.40 hours. On the other hand, the t 1/2 (lambda z)of 3H-emetine were 65.4-163 hours, which revealed a biexponential decrease. The radioactivity of both tritium-labeled compounds was distrbuted maximally in most tissues at 24 hours. For 3H-cephaeline, the maximum radioactivity levels in tissues were approximately 100-150 times greater than in plasma. For 3H-emetine, the radioactivity levels in tissues were approximately 1000-3000 times greater than in plasma. Tissue radioactivity levels decreased at a substantially slower rate than that observed in plasma. Tissue radioactivity of 3H-emetine decreased more slowly than that of 3H-cephaeline. For 3H-cephaeline, the cumulative biliary excretion of radioactivity was 57.5% at 48 hours. The cumulative urinary and fecal excretion of radioactivity in these rats was 16.5% and 29.1%, respectively, of the dose at 48 hours following dosing. For 3H-emetine, the cumulative biliary excretion of radioactivity was 12.5% at 48 hours. The cumulative urinary and fecal excretion of radioactivity was 9.4% and 34.1%, respectively, of the administered dose at 48 hours. The radioactivity level of 3H-emetine remaining in the carcasses at 48 hours was equivalent to approximately 50% of the dose. A portion of each tritium-labeled compound was subjected to entero-hepatic circulation. Thus, the absorption rate of 3H-cephaeline and 3H-emetine was estimated to be approximately 70% on the basis of the data obtained from excretion studies. There was no difference in the absorption process between these two compounds. However, the difference was admitted in the biliary clearance, which is the main excretion route of both compounds. Delayed excretion of 3H-emetine may be primarily due to its resorption as related to entero-hepatic circulation and tissue retention. This study has determined the absorption, distribution and excretion of 3H-cephaeline and 3H-emetine in rats.

Absorption↗