Disease relevance of Taurodeoxycholate

• In contrast, taurodeoxycholate caused only minimal esophagitis and no hemorrhage, but caused extensive disruption of the esophageal mucosal barrier [1].
• Taurochenodeoxycholate or taurodeoxycholate, infused intraduodenally at 24 or 16 mumols/100 g rat per hour, respectively, caused cholestasis and severe hepatocellular necrosis within 8 hours [2].
• In both systems, cytolysis increased sigmoidally with increasing bile salt concentration, and the relative toxicity of different bile salts proceeded in the following order: tauroursodeoxycholate was less toxic than taurocholate, which was less toxic than taurodeoxycholate [3].
• The crystal structures of conjugated bile acid hydrolase (CBAH) from Clostridium perfringens as apoenzyme and in complex with taurodeoxycholate that was hydrolyzed to the reaction products taurine and deoxycholate are described here at 2.1 and 1.7 A resolution, respectively [4].
• Subsequently the influence of a bile salt mixture (85% taurocholate, 15% taurodeoxycholate) on the binding and uptake of Salmonella abortus equi lipopolysaccharide by cultured rat Kupffer cells was studied [5].

High impact information on Taurodeoxycholate

• Whole-cell patch-clamp techniques and fluorescence measurements of intracellular Ca2+ concentration, (Ca2+)i, were used to investigate the mechanism of taurodeoxycholate (TDC) stimulation of Cl- secretion in the T84 colonic cell line [6].
• METHODS: Contractile responses to cholecystokinin (CCK), bethanechol, KCI, and field stimulation were constructed alone and in the presence of selected bile salts: taurodeoxycholate (TDC), taurochenodeoxycholate, taurocholate, and tauroursodeoxycholate (TUDC) [7].
• When 5 or 50 micromol/L of TUDC was added to the organ bath before the application of equalmolar TDC, the TDC-induced impaired gallbladder contractility was reversed [7].
• RESULTS: More hydrophobic bile salts, such as TDC (as low as 5 micromol/L), concentration-dependently depressed (P < 0.05) both CCK- and field stimulation-induced gallbladder contractions [7].
• Tritium-labeled taurodeoxycholate (0.5 muCi) was injected as a pulse to determine uptake, biotransformation, and hepatic secretion [8].

Chemical compound and disease context of Taurodeoxycholate

• METHODS: H. pylori isolates from patients with duodenal ulcer and from volunteers with asymptomatic gastritis (six each) were grown in brain heart infusion broth medium containing mixtures of glycocholate, taurocholate, glycodeoxycholate, taurodeoxycholate, glycochenodeoxycholate, and taurochenodeoxycholate with and without lecithin [9].
• An infusion of increasing amounts of the hydrophobic BS taurodeoxycholate increased cholesterol excretion by 3.0- and 2.4-fold in wild-type and Abcg5(-/-) mice but rapidly induced cholestasis in Abcg5(-/-) mice [10].

Biological context of Taurodeoxycholate

• We conclude that mice overexpressing Abcb11 display an increase in biliary bile salt secretion and taurodeoxycholate content, which is associated with FXR/SHP-mediated changes in hepatic and ileal gene expression [11].
• When footprint A (-101 to -49) or 7 alpha TRE (-73 to -55) sequence was linked upstream to a heterologous SV40 promoter/luciferase plasmid and transiently transfected into HepG2 cells, taurodeoxycholate suppressed the SV40 promoter activity [12].
• The expressed Na(+)-dependent taurocholate uptake exhibited saturation kinetics (apparent Km of 48 microM), and displayed similar competitive substrate inhibition by taurodeoxycholate as the native brush border Na+/bile salt co-transporter studied in pig ileal brush border membrane vesicles [13].
• Six days after exposure to taurodeoxycholate, IEC-6 cell proliferation was significantly increased [14].
• Prior studies have shown that the bile salt taurodeoxycholate increases cell migration after injury [14].

Anatomical context of Taurodeoxycholate

• Water and electrolyte absorption continued undisturbed when the gallbladders were exposed to 16.7 mM taurodeoxycholate together with 5.6 mM lecithin [15].
• We have compared the potentially injurious effect of physiologic concentrations of trypsin, taurodeoxycholate, and pepsin at pH 7.5 using a continuously perfused rabbit esophagus model [1].
• After 4 days of biliary drainage, rat livers were perfused in vitro in either forward (through the portal vein) or backward direction (through the vena cava) in single-pass arrangement with taurodeoxycholate (32 nmol.min-1.g liver-1) [8].
• The enzyme reaction was optimal above pH 5.5, and a 2-3-fold stimulation of activity was observed when the membranes were assayed in the presence of 0.1% taurodeoxycholate [16].
• Treatment of intact coated vesicles with pronase (0.05 mg/ml) had little effect on lysosomal enzyme activities, whereas a similar treatment of coated vesicles in the presence of 0.045% taurodeoxycholate resulted in the loss of most of the enzyme activities [17].

Associations of Taurodeoxycholate with other chemical compounds

• The inhibitory effect of ethanol on bile flow and BS secretion was significantly (P < .02) attenuated by perfusing liver with the hydrophilic BS, tauroursodeoxycholate (TUDCA), and it was exacerbated (P < .02) by perfusion with the hydrophobic BS, taurodeoxycholate (TDCA) [18].
• Moreover, the stimulatory effect of taurodeoxycholate on release of gallbladder glycoprotein was much reduced when it was presented in model biles rather than in aqueous solution [19].
• Taurocholate and taurodeoxycholate (50 microM) repressed cholesterol 7 alpha-hydroxylase mRNA to 44 +/- 9 and 52 +/- 4%, respectively, of control values [20].
• In the total microsomal fraction, the enzyme had a pH optimum of 7.5 and was completely inhibited by Triton X-100 and deoxycholate, but not by taurodeoxycholate and beta-octyl glucoside [21].
• The taurodeoxycholate-activated galactosylceramidase could be completely separated from the taurocholate-activated galactosylceramidase and GM1-ganglioside beta-galactosidase (EC 3.2.1.23) by octyl-Sepharose hydrophobic chromatography [22].

Gene context of Taurodeoxycholate

• Effect of intraduodenal bile and Na- taurodeoxycholate on exocrine pancreatic secretion and on plasma levels of secretin, pancreatic polypeptide, and gastrin in man [23].
• Nevertheless Cbs1p is tightly associated with the mitochondrial membrane, as shown by its behaviour in extraction experiments with taurodeoxycholate [24].
• Because these changes in gene expression are associated with an increased overall hydrophobicity of the bile salt pool and a 4-fold increase of the FXR ligand taurodeoxycholate, they reflect bile salt-mediated regulation of FXR and SHP target genes [11].
• Control mice (+/+), and mice with a homozygous (-/-) or heterozygous (+/-) disruption of the mdr2 gene, were infused with taurodeoxycholate (TDC) or tauroursodeoxycholate (TUDC) [25].
• MATERIALS AND METHODS: Transmucosal resistance and Na-fluorescein permeability of ileal mucosa segments from female Wistar rats were determined in Ussing chambers during a 30-min incubation with model systems containing: control-buffer, taurodeoxycholate (TDC), Indo, TDC-Indo, TDC-PC, or TDC-PC-Indo [26].

Analytical, diagnostic and therapeutic context of Taurodeoxycholate

• Swine livers were harvested after the intravenous infusion of 1 of 3 solutions: saline (n = 7), tauroursodeoxycholate ([TUDC] hydrophilic; n = 4), or taurodeoxycholate ([TDC] hydrophobic; n = 4) [27].
• These bile salts also reduced crystallization dose dependently after addition of taurodeoxycholate to vesicles [28].
• Cow, goat, and human globules were subjected to varying concentrations of the bile salt taurodeoxycholate at 37 degrees C for 2 min, and the released material was obtained by centrifugation at 2 degrees C and 50,000 g for 1 h [29].
• Taurochenodeoxycholate 3,7-disulphate and taurodeoxycholate 3,12-disulphate in human urine were unequivocally identified on the basis of their behavior in HPLC using mobile phases of different pH [30].
• This process of derivatization was carried out efficiently and in a nonselective manner over a period of 30 min at 90 degrees C. The resulting derivatives were separated with high resolution by capillary electrophoresis using borate buffer, containing taurodeoxycholate, as the separation buffer [31].

References