Urine Of Guinea Pigs Research Articles

On the Metabolism of Prostaglandins E1 and E2 in the Guinea Pig

Abstract 5β, 7α-Dihydroxy-11-ketotetranor-prostanoic acid was the major metabolite excreted in the urine of guinea pigs injected with tritium-labeled prostaglandin E1, prostaglandin E2, 11α,15l-dihydroxy-9-ketoprost-5-enoic acid, 11α-hydroxy-9,15-diketoprostanoic acid, and 11α-hydroxy-9,15-diketoprost-5-enoic acid. A method was developed for quantitative determination of 5β,7α-dihydroxy-11-ketotetranor-prostanoic acid in 24-hour samples of guinea pig urine. The basal excretion of the metabolite in 10 male guinea pigs was 1.34 to 2.74 µg per kg of body weight x 24 hours. Administration of 50 mg of indomethacin per day inhibited the excretion of the urinary metabolite by about 98%.

Die bildung optisch aktiver sulfoxide im stoffwechsel von p-thioanisidin

Metabolites of p-thioanisidine identified in the urine of mice, rats, guinea-pigs and rabbits contain, besides unchanged starting material, p-thioanisidine sulfoxide, p-thioanisidine sulfone and the N-acetyl derivatives and conjugates of these substances. The sulfoxides are dextro-rotary and have R-configuration on the sulfur atom. The formation of the optically active sulfoxides seems to be of indirect origin, probably because of secondary transformations of the S-isomer in vivo. The microorganism Aspergillus niger, which is known to synthesize optically active sulfoxides from thioethers, is able to reduce preferably the S-enantiomer of p-thioanisidine sulfoxide. The sulfoxidation of p-thioanisidine by mammals is a microsomal mixed function oxidation, which is not stereospecific. On the other hand rat liver microsomes oxidize S(−)- p-thioanisidine sulfoxide more rapidly than R(+)- p-thioanisidine sulfoxide. Similarly the 100 000 g supernatant of rat liver homogenate is containing a protein, which reduces predominantly S(−)- p-thioanisidine sulfoxide. Both stereoselective reactions seem to be the cause of the formation of optically active sulfoxides in vivo.

Studies on the submaxillary gland. XIV. Radioimmunoassay of parotin

In an effort to increase the sensitivity and specificity in the assay of salivary galnd hormones, a radioimmunoassay of parotin was attempted. The radioimmunoassy was carried out by incubation of a mixture of anti-parotin serum, 131I-parotin, and parotin sample, followed by separation of antibody-bound 131I-parotin (B) from free 131I-parotin (F) by paper electrophoresis with hydrodynamic flow. The radioactivity of B and F was counted, and the amount of parotin was determined by the ratio of B/F. The sensitivity was 2 mμg. Although S-parotin showed cross reaction with parotin to some extent, negative cross reactions were found for bovine serum γ-globulin and for other substances, such as the hypocalcemic substance from B. subtilis K and the MSH like substance from human which are active in decreasing calcium. This radioimmunoassay method can be used for determination of parotin present in the parotid gland, submaxillary gland, serum and urine of guinea pigs, and in urine and saliva of human, for which the previous methods of bioassay cannot be used directly. The present method confirmed that the content of the hormone in serum and urine of guinea pigs decreases suddenly after sialoadenectomy. The partial agreement between the results of the immunoassay of parotin and the bioassay is understandable from the fact that the anti-parotin serum neutralizes the hypocalcemic activity but not the leucocyte activity.

The metabolism of saccharin and the related compounds in rats and guinea pigs.

The metabolism of 35S-labeled saccharin, o-, p-toluenesulfonamide (TSA), o-and p-sulfamoylbenzoic acid (SBA) was investigated in rats and guinea pigs. Saccharin was rapidly excreted unchanged ; almost in urine in guinea pigs, while about 70% in urine and the remainder in feces in rats. It was suggested that such a difference of excretion patterns in the both animals might be due to the different absorption rate in stomach presumed from the observation of distinct pH values of their gastric juice. The urinary excretion of o-and p-TSA in rats was approximately 80% of those compounds administered, halves of which were oxidized to o-and p-SBA respectively by the oxidation of the methyl group. More than 90% of o-and p-SBA were excreted unchanged in rats, but the excretion ratios shared in urine and feces were considerably variable in individual animals.

Urinary excretion of tertiary amino methoxy methylenedioxy propiophenones as metabolites of myristicin in the rat and guinea pig.

Two nitrogen-containing metabolites of myristicin (1-methoxy-2,3-methylenedioxy-5-allyl benzene) are excreted in the urine of rats and guinea pigs following oral or intraperitoneal administration. The major basic ninhydrin-positive urinary metabolite of myristicin in the rat is 3-piperidyl-1-(3′methoxy-4′,5′-methylenedioxyphenyl)-1-propanone, while the major basic ninhydrin-positive urinary metabolite of the guinea pig is 3-pyrrolidinyl-1-(3′methoxy-4′,5′-methylenedioxyphenyl)-1-propanone. In addition, the rat and guinea pig excrete trace quantities of the pyrrolidinyl ketone and piperidyl ketone, respectively. In contrast to the urinary basic metabolites of safrole, no detectable quantity of the N , N dimethylamino ketone was present in either rat or guinea pig urine after administration of myristicin; the guinea pig upon administration of safrole excreted only the substituted 3- NN -dimethyl amino propiophenone.

Identification of tertiary aminomethylenedioxy-propiophenones as urinary metabolites of safrole in the rat and guinea pig

Three nitrogen-containing metabolites of safrole (1-allyl-3,4-methylenedioxy-benzene) are excreted in the urine of rats and/or guinea pigs following oral or intraperitoneal administration. The major safrole basic ninhydrin-positive metabolites of the guinea pig and rat are 3- N- N-dimethylamino-1-(3′,4′-methylenedioxyphenyl)-1-propanone and 3-piperidyl-1-(3′,4′-methylenedioxyphenyl)-1-propanone, respectively. In addition, the rat also excretes the above N, N-dimethylaminoketone and trace amounts of 3-pyrrolidinyl-1-(3′,4′-methylenedioxyphenyl)-1-propanone. All three of these aminoketones decompose to form 1-(3′,4−methylenedioxyphenyl)-3-propen-1-one.

Studies on trimetoquinol—I: Distribution, excretion and metabolism of trimetoquinol

Distribution, excretion and metabolism of [ 3H]trimetoquinol and [ 3H]isoproterenol in the guinea pig and rat were studied. Ten min after [ 3H]trimetoquinol was injected intravenously (i.v.) into a guinea pig, the highest concentration was found in kidney, moderate levels in spleen, lung and heart, and very low level in brain. The pattern of distribution of [ 3H]isoproterenol was similar to that of [ 3H]trimetoquinol. However, levels of [ 3H]trimetoquinol in tissues other than liver and kidney were higher than were those of [ 3H]isoproterenol. After [ 3H]trimetoquinol administration, 42 per cent of the radioactivity was excreted in 48 hr in urine and 49 per cent in 48 hr in faeces; after [ 3H]isoproterenol administration, 87 per cent of the radioactivity was excreted in the 48-hr urine. It was found that trimetoquinol, like isoproterenol, was metabolized by either O-methylation or conjugation with glucuronic acid. Of the radioactivity excreted in the 4-hr urine of guinea pigs given [ 3H]trimetoquinol, the largest part (61.0 per cent) was the glucuronide of this drug, 11.5 per cent was unchanged and the remainder was O-methylated trimetoquinol and its glucuronide. When [ 3H]isoproterenol was injected i.v. into guinea pigs, of the radioactivity in the 4 hr urine, the largest part (55.0 per cent) was the glucuronide of O-methylated isoproterenol, 10 per cent was unchanged and the remainder was either O-methylated isoproterenol or the glucuronide. Differential urinary and biliary excretion of trimetoquinol and its d-isomer was observed in both the rat and guinea pig. The O-methylation of the l- and d-isomers by liver homogenates of rat and guinea pig was relatively stereospecific for the l-isomer.

The Sda blood group antigen in tissues and body fluids.

Abstract. In man the Sdaantigen is present in most secretions with the greatest concentration in urine. There is little difference in the amount of Sdasubstance in the urine of newborn infants, pregnant women and normal adults but there is a much greater amount in the saliva of newborn infants than in adults. Approximately half the people whose red cells group as Sd(a‐) secrete Sdasubstance in the urine. Anti‐Sdaantibody is present in 50% of Sd(a‐) non‐secretors of Sdasubstance, though most of these antibodies only react with the strongest Sd(a +) cells. The greatest Sdaactivity has been found in human meconium, guinea pig urine and guinea pig kidney. Activity can be detected in the urine of many animal species. The kidneys of 5 bird species did not contain Sda.

Metabolism of drugs. LXIX. Studies on the urinary metabolites of morphine in several mammlian species.

In the previous study of this series, morphine was shown to be metabolized not only to morphine-3-glucuronide, but also to morphine-6-glucuronide in rabbits. The present study have demonstrated that this is common in rabbits, guinea pigs, rats, mice and human. As a minor metabolite of morphine, normorphine was also detected in the urine samples of these species by thin-layer chromatography. However, the excretion of this metabolite into the urine of guinea pigs given morphine was not conclusive, since the similar spot was also observed on the thin-layer chromatogram of the urine extract from untreated animals. Quantitative estimation of major metabolites of morphine in the urine of rabbits and guinea pigs indicated that most of the dose was accounted for as conjugated morphine, but in rats morphine was excreted mostly as free morphine and in lesser amount as the conjugates in 24 hr urine.

Metabolism of aflatoxin in susceptible and resistant animal species

Dietary aflatoxin B 1 was excreted in the urine of rats, goats and guinea-pigs as aflatoxin M 1, while some unchanged B 1 was excreted in the faeces. M 1 was not confirmed in the excreta of ducklings given B 1 orally but was found in the tissues of ducklings shortly after an intraperitoneal dose of B 1. Comparative studies in nine avian and mammalian species showed that there was no correlation between the known susceptibility of the different species to aflatoxin B 1 and the basal levels of hepatic microsomal enzymes (NADPH oxidase and aniline hydroxylase) or the rates of in vitro metabolism of the toxin by liver homogenates. Although liver preparations of several species metabolized aflatoxin B 1 almost completely, only minute amounts of M 1 were formed. However, an unidentified non-fluorescent metabolite (designated metabolite X) was also detected. The optimal formation of this metabolite depended on the presence of both liver microsomes and 105,000 g supernatant as well as NADPH as cofactor. The ability of liver preparations obtained from susceptible species to transform aflatoxin B 1 into products not toxic to day-old ducklings suggested that aflatoxin B 1 may exert its acute toxicity through the agency of a highly toxic and unstable metabolite.

Metabolism of drugs. LXIV. Species differences of metabolism of phenacetylurea.

In our previous papers, it was shown that phenacetylurea administered to rabbits is metabolized to 3-methoxy-4-hydroxyphenacetylurea, but in mice it is not converted to this unique metabolite. The present study revealed that the above metabolite is also excreted as one of the major metabolites in the urine of guinea pigs and a human after doses of phenacetylurea, as well as rabbits, whereas rats apparently do not follow to this pathway. Although in these species of animals and in a human the metabolic patterns of phenacetylurea were somewhat different each other, the drug was metabolized by two main pathways, hydroxylation of aromatic ring and hydrolysis of ureide group in all species examined. The identification and determination of the metabolites in animal species were facilitated by use of 14C-labeled phenacetylurea.

Imidazoleacetic acid excretion in guinea-pigs adapted to histamine

The excretion of imidazoleacetic acid (ImAA) was examined in the urine of guinea-pigs treated daily for 8–12 weeks with histamine aerosols (adapted guinea-pigs). In histamine-adapted animals tested 8 days after the last exposure to histamine aerosol, the urinary excretion of ImAA was higher than in normal ones. However, in contrast to normal animals any additional inhalation of histamine produced a marked decrease in ImAA excretion. The inhibitory action of excessive amounts of histamine on diamine oxidase (DAO) (EC. 1.4.3.6) activity and therefore ImAA excretion may depend on the formation of a condensation product of histamine with pyridoxal phosphate. The role of the inhibitory action of an excess of histamine on the original metabolic pathway of histamine degradation is discussed.

Preliminary Study of Carbohydrates in the Urine of Manganese-deficient Guinea Pigs at Birth

Carbohydrate components of urine of manganese-deficient and control newborn guinea pigs have been determined before the animals had access to extrauterine nourishment. Small amounts of the sugars arabinose, fructose, fucose, galactose, glucose, lactose, mannose, ribose and xylose were found in the urine of newborn guinea pigs of both manganese-deficient and control dams. Equating urine specimens on the basis of creatinine concentration revealed that slightly higher amounts of ribose occurred in the manganese-deficient progeny. The most striking difference in the carbohydrate components of urine was a threefold higher concentration of free myoinositol in the urine of control animals at birth. Compounds were determined by paper chromatography techniques. Some speculation is made about the reduced myoinositol content of urine of manganese-deficient young, the synthesis of glucuronic acid in fetal development, and the relation of these to connective tissue defects known to occur in manganese-deficient guinea pigs.

Species differences in the metabolism of sulphadimethoxine.

1. The fate of sulphadimethoxine (2,4-dimethoxy-6-sulphanilamidopyrimidine) was studied in man, rhesus monkey, dog, rat, guinea pig and rabbit. 2. About 20-46% of the dose (0.1g./kg.) of the drug is excreted in the urine in 24hr. in these species, except the rat, in which only 13% is excreted. 3. In man and the monkey sulphadimethoxine N(1)-glucuronide is the major metabolite in the urine. In the rabbit and guinea pig N(4)-acetylsulphadimethoxine is the main metabolite. In the dog the drug is excreted mainly unchanged. In the rat equal amounts of the unchanged drug and its N(4)-acetyl derivative are the main products. 4. Small amounts of sulphadimethoxine N(4)-glucuronide are found in the urine of all the species. Sulphadimethoxine N(1)-glucuronide occurs in small amounts in the urine of rat, dog and guinea pig; none is found in rabbit urine. 5. Sulphadimethoxine N(4)-sulphate was synthesized and found to occur in small amounts in rat urine. 6. Monkey liver homogenates fortified with UDP-glucuronic acid are able to synthesize sulphadimethoxine N(1)-glucuronide with the drug as substrate. Rat liver has also this ability to a slight extent, but rabbit liver is unable to do so. 7. Sulphadimethoxine N(4)-glucuronide is formed spontaneously when the drug is added to human urine. 8. The biliary excretion of the drug and its metabolites was examined in rats. The drug is excreted in rat bile mainly as the N(1)-glucuronide. The N(1)- and N(4)-glucuronides administered as such are extensively excreted in the bile by rats.

A method for determination of trichloroethanol and trichloroacetic acid in urine.

When trichloroacetic acid (TCA) and trichloroethanol (TCE) in the urine of human subjects, rabbits, rats, and guinea-pigs were determined by Seto and Schultze9s (1956) method, the recovery of TCE, added to urine, varied widely from 81·3% in guinea-pig urine to 16·2% in rat urine. To obtain the maximum recovery of added TCE, Seto and Schultze9s method was further modified to give satisfactory results (recovery rate of 95·9 to 98·5%) when applied to human urine as well as to the urine of the above species of animals. Urine samples from human subjects as well as from rats exposed to trichloroethylene were analysed by this modified method. The results showed that the ratio of TCE to TCA varies as a function of environmental trichloroethylene concentration, indicating that the determination of total trichlorocompounds gives a better index of trichloroethylene exposure than does the determination of TCA alone.

17-Hydroxycorticosteroid excretion rhythms in guinea pigs

ARTICLES17-Hydroxycorticosteroid excretion rhythms in guinea pigsWH HuibregtseWH HuibregtsePublished Online:01 Jun 1968https://doi.org/10.1152/ajplegacy.1968.214.6.1268MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByDetermination of cortisol in guinea pig urine by high performance thin-layer chromatography, high performance liquid chromatography, and thin-layer chromatography/radioimmunoassayChromatographia, Vol. 44, No. 1-2Thin-layer chromatography on silica-coated aluminium sheet as an adjunct to radioimmunoassay of steroidsJournal of Chromatography B: Biomedical Sciences and Applications, Vol. 563, No. 1Urinary excretion of free glucocorticosteriods and testosterone in the Mongolian gerbil (Meriones unguiculatus): Effects of long-acting corticotrophin and human gonadotrophinComparative Biochemistry and Physiology Part A: Physiology, Vol. 91, No. 4Secretion of corticosterone in vitro by normothermic and hibernating ground squirrelsComparative Biochemistry and Physiology Part A: Physiology, Vol. 38, No. 4 More from this issue > Volume 214Issue 6June 1968Pages 1268-1272 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.214.6.1268PubMed4870148History Published online 1 June 1968 Published in print 1 June 1968 Metrics

Metabolism of aminonucleoside-8- 14C in the rat and guinea pig

The aminonucleoside (PA) of puromycin is nephrotoxic to rats but not to guinea pigs. That guinea pigs are resistant to PA-nephrotoxicity has been confirmed in the Hartley strain. The metabolic disposition of subcutaneoulsy administered PA in the rat and in the Hartley guinea pig has been determined with the aid of the 8- 14C-labeled compound. Unchanged PA is the major urinary excretion product in both the rat and guinea pig 8 hr after PA administration, and allantoin represents the major end-product of metabolism. Guinea pigs, but not rats, excrete part of the PA-8- 14C as 14CO 2. The monodemethylated analog of PA, viz., 6-methylamino-9-(3′-amino-3′-deoxy-β- d-ribofuranosyl)purine, is the major nucleoside metabolite in the urine of rats and guinea pigs. The rat demethylates PA to this monodemethylated analog in vivo at a rate approximately 4-fold greater than the guinea pig.

Fate of unejaculated spermatozoa.

THE production of spermatozoa does not cease in sexually inactive males1–3, and it becomes necessary to examine the means of disposal of the surplus spermatozoa. The two most likely ways are either that they are voided in the urine or that they are resorbed in the epididymis or vas deferens. Early workers favoured the first of these mechanisms because they found spermatozoa in the urine of rats, guinea-pigs, dogs, and men4,5. In 1931, however, Simeone and Young1 reported that the vas deferens of the guinea-pig contained large numbers of degenerating spermatozoa and, as only small numbers of sperm were found in the urine, they concluded that resorption was the principal mechanism for disposing of the surplus spermatozoa.

Excretion of N-hydroxy-2-aminofluorene by guinea pigs injected with 2-acetylaminofluorene

Small amounts of N-hydroxy-2-aminofluorene were observed in the urine of guinea pigs intraperitoneally injected with 2-acetyl-aminofluorene. The N-hydroxylation product was identified and determined after being oxidized to 2-nitrosofluorene. After the injection of 122.8 mg as well as 245.6 mg/kg 0.03 per cent of the dose was found in the urine as N-hydroxy-2-aminofluorene.

The biochemistry of aromatic amines. The metabolism of 2-naphthylamine and 2-naphthylhydroxylamine derivatives.

1. 2-Naphthylhydroxylamine and 2-nitrosonaphthalene were present in urine of dogs but not of guinea pigs, hamsters, rabbits or rats dosed with 2-naphthylamine. N-Acetyl-2-naphthylhydroxylamine and its O-sulphonic acid and O-glucosiduronic acid were not detected in the urine of any of these species. 2. Bile from rats dosed with 2-naphthylamine contained (2-naphthylamine N-glucosid)uronic acid and 6- and 5,6-substituted derivatives of 2-acetamidonaphthalene. 2-Amino-1-naphthyl and 2-acetamido-1-naphthyl derivatives, 2-naphthylhydroxylamine and its N-acetyl derivative or conjugates of these were not detected. Bile from a dog dosed with 2-naphthylamine contained no 2-amino-1-naphthyl derivatives. 3. 2-Naphthylhydroxylamine was metabolized by the dog, rat and guinea pig to the same products as those formed by these species from 2-naphthylamine. Rabbits formed mainly 2-amino-1-naphthyl derivatives; these are minor metabolites of 2-naphthylamine in this species. 4. (N-Acetyl-2-naphthylhydroxylamine O-glucosid)uronic acid was excreted in the urine and the bile of rats and in the urine of guinea pigs and rabbits dosed with N-acetyl-2-naphthylhydroxylamine. 5. After the administration of 2-acetamidonaphthalene, (N-acetyl-2-naphthylhydroxylamine O-glucosid)uronic acid was detected in the urine of dogs, but not in the urine of other species. The dog excreted an acid-labile cysteine derivative of 2-acetamidonaphthalene, but only traces of the corresponding mercapturic acid. 6. After dosing with N-acetyl-2-naphthylhydroxylamine-O-sulphonic acid, rats excreted derivatives of 2-amino-1-naphthol. 7. 2-Nitrosonaphthalene, N-acetyl-2-naphthylhydroxylamine, N-acetyl-2-naphthylhydroxylamine-O-sulphonic acid, 2-naphthylhydroxylamine-N-sulphonic acid, N-benzyloxycarbonyl-2-naphthylhydroxylamine and N-benzyloxycarbonyl-2-naphthylhydroxylamine-O-sulphonic acid were synthesized.