scholarly journals The metabolism of potassium dodecyl [35S]-sulphate in the rat

1969 ◽  
Vol 111 (1) ◽  
pp. 43-51 ◽  
Author(s):  
W. H. B. Denner ◽  
A H Olavesen ◽  
Gillian M. Powell ◽  
K S Dodgson
Keyword(s):  
Butyric Acid ◽  
Liver Perfusion ◽  
Paper Electrophoresis ◽  
Whole Body ◽  
Hydroxybutyric Acid ◽  
Metabolic Fate ◽  
Anaesthetized Rats ◽  
Dilution Experiments ◽  
Free Ranging ◽  
Isolated Liver

The metabolic fate of potassium dodecyl [35S]sulphate was studied in rats. Intraperitoneal and oral administration of the ester into free-ranging animals were followed by the excretion of the bulk of the radioactivity in the urine within 12hr., approximately 17% being eliminated as inorganic [35S]sulphate. Similar results were obtained in experiments in which potassium dodecyl [35S]sulphate was injected intravenously into anaesthetized rats with bile-duct and ureter cannulae. Analysis of urinary radioactivity revealed the presence of a new ester sulphate (metabolite A). This metabolite was isolated, purified and subsequently identified as the sulphate ester of 4-hydroxybutyric acid by paper, thin-layer and gas chromatography, by paper electrophoresis and by comparison of its properties with those of authentic butyric acid 4-sulphate. The identity of the metabolite was confirmed by isotope-dilution experiments. When either purified metabolite A or authentic potassium butyric acid 4[35S]-sulphate was administered to free-ranging rats the bulk of the radioactivity was eliminated unchanged in the urine within 12hr., approx. 20% of the dose appearing as inorganic [35S]sulphate. Whole-body radioautography and isolated-liver-perfusion experiments implicated the liver as the major site of metabolism of potassium dodecyl [35S]sulphate. It is suggested that butyric acid 4-sulphate probably arises by ω-oxidation of dodecyl sulphate to a fatty acid-like compound, which is then degraded by β-oxidation.

scholarly journals The metabolism of labelled hexadecyl sulphate salts in the rat, dog and human

1975 ◽  
Vol 148 (2) ◽  
pp. 219-225 ◽  
Author(s):  
I Merits
Keyword(s):  
The Other ◽  
Hydroxybutyric Acid ◽  
Metabolic Fate ◽  
Main Metabolite ◽  
Rat Urine ◽  
Glycollic Acid ◽  
Dilution Experiments ◽  
Solvent Systems ◽  
A Minor ◽  
Sulphate Salts

The metabolic fate of [1-14-C]hexadecylsulphate and hexadecyl[35-S]sulphate, administered intravenously as the sodium and trimethylammonium salt to dogs and orally as the erythromycin salt to dogs, rats and humans, was studied. Studies with rats indicated that the compounds were well absorbed and rapidly excreted in the urine. However, after oral administration of the 14-C-and 35-S-labelled hexadecyl sulphate erythromycin salt to dogs, considerable amounts of radioactivity were excreted in the faeces as unmetabolized hexadecyl sulphate. Studies with two humans showed that orally administered erythromycin salt of [1-14C]hexadecyl sulphate was well absorbed in one person but poorly absorbed in the other. Radioactive metabolites in urine were separated by t.l.c. in two solvent systems. The main metabolite of hexadecyl sulphate in the dog, rat and human was identified as the sulphate ester of 4-hydroxybutyric acid. In addition, psi-[14-C]butyrolactone as a minor metabolic product of [1-14-C]hexadecyl sulphate was also isolated from the urine of rat, dog and man. However, there was still another metabolite in dog urine, which comprised about 20% of the total urinary radioactivity and carried both 14-C and 35-S labels. This metabolite was absent from rat urine. The metabolite in dog urine was isolated and subsequently identified by t.l.c. and g.l.c. and by isotope-dilution experiments as the sulphate ester of glycollic acid. Small amounts (about 5% of the total recovered radioactivity in excreta) of labelled glycollic acid sulphate were also found in human urine after ingestion of erythromycin [1-14-C]hexadecyl sulphate.

scholarly journals The metabolism of dipotassium 2-hydroxy-5-nitrophenyl [35S]sulphate, a substrate for lysosomal arylsulphatases A and B

1967 ◽  
Vol 105 (3) ◽  
pp. 1003-1012 ◽  
Author(s):  
T. G. Flynn ◽  
K S Dodgson ◽  
G M Powell ◽  
F A Rose
Keyword(s):  
Bile Duct ◽  
Kidney Function ◽  
Intraperitoneal Injection ◽  
Chromogenic Substrate ◽  
Metabolic Fate ◽  
Isolated Rat Liver ◽  
Anaesthetized Rats ◽  
Free Ranging ◽  
Rat Livers ◽  
Isolated Rat

The metabolic fate of dipotassium 2-hydroxy-5-nitrophenyl [35S]sulphate ([35S]NCS), a chromogenic substrate for lysosomal arylsulphatases A and B, has been studied in rats. Intraperitoneal injection of [35S]NCS into free-ranging animals is followed by excretion of the bulk of the radioactivity in the urine within 24hr., less than 13% being eliminated as inorganic [35S]sulphate. Most of the urinary radioactivity can be accounted for as [35S]NCS, but small amounts of a labelled metabolite are also present. Experiments in which [35S]NCS was injected intravenously into anaesthetized rats with bile-duct and bladder cannulae confirm that the ester is rapidly excreted in the urine. However, small amounts of radioactivity appear in bile, mainly in the form of the metabolite detected in urine. When [35S]NCS is perfused through the isolated rat liver, about 35% of the dose is hydrolysed within 3hr. Similar results are obtained if [35S]NCS is injected into anaesthetized rats in which kidney function has been eliminated by ligature of the renal pedicles. The labelled metabolite has been isolated from bile obtained by perfusing several rat livers with blood containing a total of 100mg. of [35S]NCS. It has been identified as 2-β-glucuronosido-5-nitrophenyl [35S]sulphate. The implications of the various findings are discussed. The Appendix describes the preparation of [35S]NCS.

scholarly journals The catabolism of intravenously injected heparan N-[35S]sulphate in the rat

1977 ◽  
Vol 166 (3) ◽  
pp. 373-379 ◽  
Author(s):  
Martin A. Perry ◽  
Gillian M. Powell ◽  
Frederick S. Wusteman ◽  
C. Gerald Curtis
Keyword(s):  
Heparan Sulphate ◽  
The Body ◽  
Whole Body ◽  
General Distribution ◽  
In Vitro Experiments ◽  
Metabolic Fate ◽  
Inorganic Sulphate ◽  
Anaesthetized Rats

The metabolic fate of heparan N-[35S]sulphate was studied in rats. Heparan sulphate was obtained from either bovine aorta or lung and labelled with 35S by desulphation and subsequent resulphation in vitro. Experiments in which heparan N-[35S]sulphate was administered intravenously to either free-range or wholly anaesthetized rats with ureter cannulae established that substantial desulphation occurs in vivo, with elimination of inorganic [35S]sulphate in urine. Oligosaccharides labelled with 35S, possible intermediates in heparan sulphate degradation, could not be detected in urine or blood. The general distribution of radioactivity after administration of heparan N-[35S]sulphate, as demonstrated by whole-body radioautography, suggested that desulphation was not restricted to one organ in particular. Support for this view was obtained in experiments in which heparan N-[35S]sulphate was administered to animals after the removal of kidneys, liver, spleen, pancreas or gastrointestinal tract. In all cases inorganic [35S]sulphate was still produced. The ability of rats of desulphate heparan N-[35S]sulphate was progressively impaired by increasing concentrations of heparin administered simultaneously. It was concluded that heparan sulphate is metabolized at a number of sites in the body by a sequence of degradative events leading to the formation of inorganic sulphate. It is also concluded that at least some of these events are common to heparan sulphate and heparin.

scholarly journals Liver and tumour tissue concentrations of TNF-alpha in cancer patients treated with TNF-alpha and melphalan by isolated liver perfusion

1997 ◽  
Vol 75 (10) ◽  
pp. 1497-1500 ◽  
Author(s):  
PJK Kuppen ◽  
LE Jonges ◽  
CJH van de Velde ◽  
AL Vahrmeijer ◽  
RAME Tollenaar ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Liver Perfusion ◽  
Tumour Tissue ◽  
Tnf Alpha ◽  
Tissue Concentrations ◽  
Isolated Liver Perfusion ◽  
Isolated Liver

scholarly journals Quantitative Analysis of the Whole-Body Metabolic Fate of Branched-Chain Amino Acids

2019 ◽  
Vol 29 (2) ◽  
pp. 417-429.e4 ◽  
Author(s):  
Michael D. Neinast ◽  
Cholsoon Jang ◽  
Sheng Hui ◽  
Danielle S. Murashige ◽  
Qingwei Chu ◽  
...  
Keyword(s):  
Amino Acids ◽  
Quantitative Analysis ◽  
Branched Chain Amino Acids ◽  
Whole Body ◽  
Metabolic Fate ◽  
Branched Chain

scholarly journals The Elution of 51Cr from Labelled Leukocytes —a New Theory

Blood ◽  
1969 ◽  
Vol 33 (3) ◽  
pp. 408-413 ◽  
Author(s):  
PETER M. RONAI
Keyword(s):  
Covalent Bond ◽  
Paper Electrophoresis ◽  
Cellular Protein ◽  
Whole Body ◽  
Trichloracetic Acid ◽  
Protein Fragments ◽  
Body Counting ◽  
Whole Body Counting

Abstract Chromium-51 elutes rapidly from labelled leukocytes and tumor cells both in vitro and in vivo. Eluted 51Cr is dialysable and is not precipitated with trichloracetic acid and it has therefore been assumed to be free chromium which has dissociated from the labelled cellular protein. In vitro studies with 51Cr-labelled albumin have, however, demonstrated the extreme stability of the covalent bond between chromium and protein. Paper electrophoresis experiments are here described which show that the 51Cr which elutes from labelled mouse peritoneal cells behaves electrophoretically like 51Cr-labelled peptides and not at all like free 51Cr in either hexavalent or trivalent forms, or 51Cr-labelled lysine and arginine. Whole body counting studies after the intravenous injection of the various 51Cr preparations into mice indicate that eluted 51Cr and 51Cr-labelled peptides also have similar biologic behavior. Together, the electrophoretic and whole body counting studies exclude the presence of significant amounts of free 51Cr (either hexavalent or trivalent) in the 51Cr that elutes from labelled cells and supports the hypothesis that 51Cr elution results from turnover of labelled protein within the cell and loss of non-reutilisable labelled protein fragments. Confirmation of this theory would provide a powerful technic for the study of intra and extracellular protein metabolism.

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