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PubMedDate not supplied

Hepatic transport of sulfated and nonsulfated bile acids in the rat following relief of bile duct obstruction.

The effect of bile duct ligation for 5 days on the hepatic transport of sulfated and nonsulfated bile acids was studied. Tracer doses of radioactive bile acids [3H]taurochenodeoxycholate-3-sulfate [3H]chenodeoxycholate-3-sulfate, [3H]taurochenodeoxycholic acid and [14C]taurocholic acid were injected 90 min after relief of obstruction when the plasma total bile acid concentration had reverted to normal. Plasma clearance and biliary excretion of sulfated bile acids were lower than those of nonsulfated bile acids, particularly in the cholestatic rats (p less than 0.02). For each bile acid, hepatic transport in the cholestatic rats was significantly reduced compared with the control rats. [3H]Chenodeoxycholate-3-sulfate and [3H]taurochenodeoxycholic acid were partially metabolized to [3H]taurochenodeoxycholate-3-sulfate prior to biliary excretion. This data suggests that the hepatic transport system for sulfated bile acids is less efficient and more easily impaired by cholestasis than that for nonsulfated bile acids.

Animals↗

PubMed1985

The availability of different sources of cholesterol for bile acid synthesis by cultured chick embryo hepatocytes.

The availability of different sources of cholesterol for bile acid synthesis by cultured chick embryo hepatocytes was studied. Mevalonolactone was taken up by the cells and converted to cholesterol, cholesterol ester and tauroconjugates of bile acids. The addition of mevalonolactone had little effect on the conversion of endogenous cholesterol to taurocholic acid; however, taurochenodeoxycholic acid synthesis was stimulated. 25-30% of the cholesterol synthesized from mevalonolactone was converted to taurochenodeoxycholic, taurocholic and two so-far unidentified bile acids. All bile acids were secreted into the incubation medium. When cholesterol was added as mixed liposomes with phosphatidylcholine, it was taken up by the cells and converted to bile acids. At low concentrations of liposomes, the greater part of the cholesterol which was taken up by the cells was converted to bile acids. At higher concentrations, considerable amounts of cholesterol and cholesterol ester accumulated inside the cells. When mevalonolactone and cholesterol liposomes was added together, both substrates were used simultaneously for bile acids synthesis. HDL cholesterol was the best substrate tested, yielding large amounts of two, so-far, unidentified bile acids (possibly allo-bile acids) and smaller amounts of taurocholic and taurochenodeoxycholic acid. Addition of HDL suppressed the conversion of endogenous cholesterol to taurocholic acid; taurochenodeoxycholic acid synthesis, however, was stimulated.

Acetates↗

PubMed2005

Phosphatidylinositol 3-kinase-dependent signaling modulates taurochenodeoxycholic acid-induced liver injury and cholestasis in perfused rat livers.

Taurochenodeoxycholic acid (TCDCA), but not glycochenodeoxycholic acid (GCDCA), activates a phosphatidylinositol 3-kinase (PI3-K)-mediated survival pathway in vitro. Here, the effects of PI3-K inhibition on TCDCA- and GCDCA-induced hepatocellular injury, apoptosis, and bile secretion were examined in the intact liver. In isolated perfused rat livers, bile flow was determined gravimetrically. Hepatovenous lactate dehydrogenase and alanine aminotransferase efflux as markers of liver integrity and biliary secretion of 2,4-dinitrophenyl-S-glutathione (DNP-GS) were determined photometrically. Apoptosis was assessed by immunohistochemistry of active caspase-3 and cytokeratin 18 in liver tissue. Phosphorylation of protein kinase B (PKB/Akt) as a readout of PI3-K activity was determined by immunoblot analysis. Bile acid concentrations were determined by gas chromatography. TCDCA (25 muM) induced moderate liver injury by hepatocellular apoptosis and distinctly reduced bile flow and DNP-GS secretion. In contrast, GCDCA (25 muM) induced severe liver injury by extensive hepatocyte apoptosis. TCDCA strongly activated PI3-K, whereas GCDCA did not markedly affect PI3-K activity. Inhibition of PI3-K by 100 nM wortmannin enhanced TCDCA-induced liver injury and apoptosis and tended to aggravate the cholestatic effect of TCDCA. In contrast, wortmannin reduced GCDCA-induced liver injury and apoptosis. Bile acid uptake tended to be reduced by wortmannin. The cholestatic effect of GCDCA was aggravated by wortmannin. Inhibition of PI3-K markedly aggravated TCDCA-induced but not GCDCA-induced liver damage and hepatocyte apoptosis. Thus TCDCA appears to block its inherent toxicity by a PI3-K-dependent survival pathway in the intact liver.

Androstadienes↗

PubMed2006

Single-step analysis of individual conjugated bile acids in human bile using 1H NMR spectroscopy.

1H and 13C NMR spectra of intact human bile were assigned using one-dimensional (1H and 13C) and two-dimensional (1H-1H and 1H-13C) experiments. Individual conjugated bile acids--glycocholic acid, glycodeoxycholic acid, glycochenodeoxycholic acid, taurocholic acid, taurodeoxycholic acid, and taurochenodeoxycholic acid--were identified. The bile acids were quantified accurately and individually in a single step by using distinct and characteristic amide signals. Making use of 13C NMR, the study also suggests a way to analyze unconjugated bile acids separately, if present. Chemical shift assignments and rapid single-step analysis of individual conjugated bile acids from intact bile presented herein may have immense utility in the study of bile acid metabolism and deeper understanding of hepatobiliary diseases.

Bile↗

PubMed1985

Inhibition of pepsin activity by ursodeoxycholic acids and chenodeoxycholic acids.

The bile salts of ursodeoxycholic acid, glycoursodeoxycholic acid, tauroursodeoxycholic acid, chenodeoxycholic acid, glycochenodeoxycholic acid, and taurochenodeoxycholic acid were each found to inhibit pepsin proteolytic activity in vitro at various concentrations against the refined substrate n-APDT. The sodium salt of ursodeoxycholic acid was the most potent pepsin inhibitor among those tested.

Animals↗

PubMed2002

High metabolic function of primary human and porcine hepatocytes in a polyurethane foam/spheroid culture system in plasma from patients with fulminant hepatic failure.

It has been demonstrated that plasma from patients with fulminant hepatic failure (FHF) interferes extensively with cellular function. We placed primary human and primary porcine hepatocytes in a polyurethane foam (PUF)/spheroid culture system and compared the metabolic functions in the plasma of patients with FHF in a 24-h stationary culture to those in a monolayer culture. The PUF/spheroid culture system using primary human and primary porcine hepatocytes significantly decreased ammonia content during 28-day culture. Fisher's ratio significantly increased at culture days 3 and 7. Tauroursodeoxycholic acid significantly increased and glycochenodeoxycholic acid and taurochenodeoxycholic acid decreased in the FHF patients' plasma at culture day 3. During at least a 24-h culture in the FHF patients' plasma, metabolic functions of primary human and primary porcine hepatocytes were almost identical. The present results indicate that the PUF/spheroid culture system using primary human or primary porcine hepatocytes demonstrated more advantageous metabolic functions in the plasma from patients with FHF than the monolayer culture.

Ammonia↗

PubMed1988

Separate transport systems for biliary secretion of sulfated and unsulfated bile acids in the rat.

Biliary secretion of 3 alpha-sulfated bile acids has been studied in Wistar rats with an autosomal recessive defect in the hepatic transport of bilirubin. Liver function, established by measurement of various enzymes in plasma, by enzyme histochemical methods, and by electron microscopy, appeared to be normal in these rats. Serum levels of unconjugated, monoglucuronidated, and diglucuronidated bilirubin were 0.62, 1.62, and 6.16 mumol/liter, respectively, compared with 0.17, 0.08, and 0.02 mumol/liter in control rats. Biliary bilirubin secretion was strongly reduced in the mutant animals: 0.21 +/- 0.03 vs. 0.39 +/- 0.03 nmol/min per 100 g body wt in control rats. Despite normal biliary bile acid output, bile flow was markedly impaired in the mutant animals, due to a 53% reduction of the bile acid-independent fraction of bile flow. The transport maximum for biliary secretion of dibromosulphthalein (DBSP) was also drastically reduced (-53%). Biliary secretion of intravenously administered trace amounts of the 3 alpha-sulfate esters of 14C-labeled taurocholic acid (-14%), taurochenodeoxycholic acid (-39%), taurolithocholic acid (-73%), and glycolithocholic acid (-91%) was impaired in the jaundiced rats compared with controls, in contrast to the biliary secretion of the unsulfated parent compounds. Hepatic uptake of sulfated glycolithocholic acid was not affected in the jaundiced animals. Preadministration of DBSP (15 mumol/100 g body wt) to normal Wistar rats significantly impaired the biliary secretion of sulfated glycolithocholic acid, but did not affect taurocholic acid secretion. We conclude that separate transport systems in the rat liver exist for biliary secretion of sulfated and unsulfated bile acids; the sulfates probably share secretory pathways with the organic anions bilirubin and DBSP. The described genetic defect in hepatic transport function is associated with a reduced capacity to secrete sulfated bile acids into bile; this becomes more pronounced with a decreasing number of hydroxyl groups on the sulfated bile acid's molecule.

Animals↗

PubMed2003

Resistance of rat hepatocytes against bile acid-induced apoptosis in cholestatic liver injury is due to nuclear factor-kappa B activation.

BACKGROUND/AIMS: To examine the extent and mechanisms of apoptosis in cholestatic liver injury and to explore the role of the transcription factor nuclear factor-kappa B in protection against bile acid-induced apoptosis. METHODS: Cholestatic liver injury was induced by bile duct ligation in Wistar rats. Furthermore, primary cultures of rat hepatocytes were exposed to glycochenodeoxycholic acid (GCDCA), tauroursodeoxycholic acid (TUDCA), taurochenodeoxycholic acid (TCDCA) and to cytokines. Apoptosis was determined by TUNEL-staining, active caspase-3 staining, activation of caspase-8, -9 and -3. RESULTS: Limited hepatocyte apoptosis and an increased expression of NF-kappaB-regulated anti-apoptotic genes A1 and cIAP2 were detected in cholestatic rat livers. Bcl-2 expression was restricted to bile duct epithelium. In contrast to TCDCA and TUDCA, GCDCA induced apoptosis in a Fas-associated protein with death domain (FADD)-independent pathway in hepatocytes. Although bile acids do not activate NF-kappaB, NF-kappaB activation by cytokines (induced during cholestasis) protected against GCDCA-induced apoptosis in vitro by upregulating A1 and cIAP2. CONCLUSIONS: GCDCA induces apoptosis in a mitochondria-controlled pathway in which caspase-8 is activated in a FADD-independent manner. However, bile acid-induced apoptosis in cholestasis is limited. This could be explained by cytokine-induced activation of NF-kappaB-regulated anti-apoptotic genes like A1 and cIAP2.

Adaptor Proteins, Signal Transducing↗

PubMed1993

Selective composition of biliary phosphatidylcholines is affected by secretion rate but not by bile acid hydrophobicity.

Little is known about the mechanisms of: 1) biliary phosphatidylcholine (PC) secretion by the hepatocyte, 2) selectivity for biliary 1-palmitoyl-2-linoleoyl-PC (PLPC) secretion, and 3) exclusion of 1-stearoyl-2-arachidonyl-PC (SAPC) from bile. The experiments were designed to determine, in rats, whether selectivity (for PLPC and against SAPC) is influenced by bile acid hydrophobicity or secretion rate. We examined the effects of bile acid depletion and of ileal infusion of taurocholic acid, tauroursodeoxycholic acid, and taurochenodeoxycholic acid. Compared to bile acid depletion, infusion of each bile acid caused PLPC to decrease from 59% of bile PC to 48%, and SAPC to increase from 2.6% to 5%. Bile acid hydrophobicity had no effect on PC selectivity, but selectivity decreased to a moderate degree as total PC secretion increased. To determine whether selectivity is for preformed molecular species, we used a new method to isotopically label four species of hepatic PC. This was done by intravenous injection of PLPC and SAPC labeled in the linoleate (14C) and arachidonate (3H) moieties. Assuming rapid mixing of each PC species in the hepatocyte as supported by the specific activity data, bile SAPC and SLPC were derived entirely from hepatic preformed SAPC and SLPC; bile PLPC was from both preformed PLPC (55%) and an unlabeled input (45%, probably direct secretion of newly synthesized PLPC). In conclusion, the selective composition of bile PC is not related to bile acid hydrophobicity, but is partially lost as secretion increases within the physiologic range.

Animals↗

PubMed1983

A radioimmunoassay for tauro-beta-muricholic acid suitable for use with isolated rat liver cells.

A new radioimmunoassay which can be used to measure the amounts of tauro-beta-muricholic acid produced by isolated rat hepatocytes in vitro is described. Cross reactivities of other bile acids known to be present in rat liver with the antiserum used in the assay were not sufficient to interfere with the measurement of tauro-beta-muricholic acid. Exogenous taurochenodeoxycholic acid was metabolised by isolated rat hepatocytes concurrently with the appearance of tauro-beta-muricholic acid in the cell.

Animals↗

PubMed2004

Effects of secretagogues and bile acids on mitochondrial membrane potential of pancreatic acinar cells: comparison of different modes of evaluating DeltaPsim.

In this study, we investigated the effects of secretagogues and bile acids on the mitochondrial membrane potential of pancreatic acinar cells. We measured the mitochondrial membrane potential using the tetramethylrhodamine-based probes tetramethylrhodamine ethyl ester and tetramethylrhodamine methyl ester. At low levels of loading, these indicators appeared to have a low sensitivity to the uncoupler carbonyl cyanide m-chlorophenylhydrazone, and no response was observed to even high doses of cholecystokinin. When loaded at high concentrations, tetramethylrhodamine methyl ester and tetramethylrhodamine ethyl ester undergo quenching and can be dequenched by mitochondrial depolarization. We found the dequench mode to be 2 orders of magnitude more sensitive than the low concentration mode. Using the dequench mode, we resolved mitochondrial depolarizations produced by supramaximal and by physiological concentrations of cholecystokinin. Other calcium-releasing agonists, acetylcholine, JMV-180, and bombesin, also produced mitochondrial depolarization. Secretin, which employs the cAMP pathway, had no effect on the mitochondrial potential; dibutyryl cAMP was also ineffective. The cholecystokinin-induced mitochondrial depolarizations were abolished by buffering cytosolic calcium. A non-agonist-dependent calcium elevation induced by thapsigargin depolarized the mitochondria. These experiments suggest that a cytosolic calcium concentration rise is sufficient for mitochondrial depolarization and that the depolarizing effect of cholecystokinin is mediated by a cytosolic calcium rise. Bile acids are considered possible triggers of acute pancreatitis. The bile acids taurolithocholic acid 3-sulfate, taurodeoxycholic acid, and taurochenodeoxycholic acid, at low submillimolar concentrations, induced mitochondrial depolarization, resolved by the dequench mode. Our experiments demonstrate that physiological concentrations of secretagogues and pathologically relevant concentrations of bile acids trigger mitochondrial depolarization in pancreatic acinar cells.

Animals↗

PubMed1986

Demonstration of a transcellular vesicle pathway for biliary excretion of inulin in rat liver.

We tested the hypothesis that the blood to bile transport of hydrophilic inert nonelectrolytes such as inulin is mediated in part by a transcellular pathway involving endosomelike vesicles (transcytosis). Forty minutes after intravenous injection of [3H]methoxyinulin into renal pedicle ligated rats, 0.8% of the radioactivity was recovered in liver homogenate and 85% +/- 3.6% of this radioactivity was associated with membrane bound vesicles. Subcellular fractionation studies and electron microscopy confirmed this association. If rats were treated with taurochenodeoxycholic acid, 5 mumol/100 g body wt, the hepatocellular uptake of [3H]methoxyinulin increased approximately twofold and [3H]methoxyinulin was again recovered in small subcellular vesicles. Furthermore, taurochenodeoxycholic acid also stimulated the biliary excretion of [3H]methoxyinulin, which peaked in bile at 20 min. Taurochenodeoxycholic acid had similar effects on the biliary excretion of horseradish peroxidase, a protein known to be transported from blood to bile by membrane vesicles. Thus under the conditions of these experiments, the dihydroxy bile acid taurochenodeoxycholic acid can stimulate the rate of vesicle-dependent transcellular transport into bile. If inulin clearance represents a maximal estimate of this process, only 6%-8% of total bile production in the rat under basal conditions would be mediated by vesicle-mediated transcytosis.

Animals↗

PubMed1981

Effect of bile acid derivatives on taurine biosynthesis and extracellular slime production in encapsulated Staphylococcus aureus S-7.

Various bile acids were added to cultures of encapsulated strains of Staphylococcus aureus growing in serum-soft agar medium of brain heart infusion broth. We examined effects of these compounds on cellular characteristics such as growth type, cell volume index, clumping factor reaction, slime yield, taurine content, and L-(--)-cysteic acid decarboxylase activity. Upon addition to the medium of either taurochenodeoxycholic acid, taurocholic acid (25 to 50 microgram/ml), or cholic acid (10 to 25 microgram/ml), the colonial morphology of taurine-positive cells (strain S-7) was altered from the diffuse to the compact type in serum-soft agar. Also, the titer of the clumping factor reaction increased, while the cell volume index and slime yield were markedly decreased. Tauro-bile acids, including taurocholic acid, taurochenodeoxycholic acid, taurodehydrocholic acid, and taurodeoxycholic acid (50 microgram/ml) inhibited the synthesis of taurine and resulted in decreased L-(--)-cysteic acid decarboxylase activity. Among all of the derivatives cholic acid itself was found to inhibit slime production and L-(--)-cysteic acid decarboxylase activity to the greatest extent. Glyco-bile acid derivatives and taurolicholic acid (50 to 100 microgram/ml) had no effect on L-(--)-cysteic acid decarboxylase activity. Compounds such as glycodeoxycholic acid (50 to 100 microgram/ml) had no effect upon any of the cellular characteristics tested. No effect was observed upon addition of any of these compounds to cultures of the taurine-negative strain (T-26-B). We did find a correlation between the inhibition of taurine biosynthesis and decreased slime production. Electron micrographs indicated that this encapsulated strain was converted to an unencapsulated state in the presence of bile acids.

Bile Acids and Salts↗

PubMed2000

Mechanism for the prevention of cholestasis involving cytochrome P4503A overexpression.

BACKGROUND: To clarify the preventive effect of taurohyodeoxycholic acid on liver cholestasis induced by toxic bile acids in rats, we evaluated whether modulation of cytochrome P4503A-linked oxidases is involved in the hepatic bile acid retention and secretion mechanism. We investigated whether the safe or the toxic taurochenodeoxycholic acid, administered singly or together, affects cytochrome P450-catalyzed drug metabolism or biliary parameters. We also considered whether the inhibition of the P-glycoprotein export pump by vinblastine might be related to cytochrome P4503A overexpression. METHODS: Hydroxylation of testosterone and N-demethylation of aminopyrine were studied in subcellular rat liver preparations after intravenous infusion of hepatoprotective and toxic bile acids administered singly or together. Bile flow, calcium secretion, biliary enzymes activity, and secretion rates of the endogenous and administrated bile acids were determined. CYP3A-dependent monooxygenases were also measured in the same coinfusion model in the presence of vinblastine. RESULTS: Although wide modulation of the activities of different P450 subfamily of isoenzymes was seen, P4503A-associated monooxygenases showed similar patterns in the various situations, i.e., induction by taurohyodeoxycholic acid, reduction by taurochenodeoxycholic acid, and protection (intermediate induction) in the coinfusion experiments. This correlates well with biliary parameters demonstrating the hepatoprotective ability of taurohyodeoxycholic acid. Coadministration of bile acids and vinblastine significantly modifies CYP3A-linked activities. CONCLUSIONS: Bile acid structure seems to be linked with hepatotoxicity/hepatoprotection and P4503A modulation. Taurohyodeoxycholic acid could be therapeutic in cholestatic liver disease by inducing P4503A; we can hypothesize that an associated P-glycoprotein expression might facilitate biliary excretion of toxic taurochenodeoxycholic acid accumulated in the liver during cholestasis.

Animals↗

PubMed1989

Role of primary and secondary bile acids as feedback inhibitors of bile acid synthesis in the rat in vivo.

The effect of various primary and secondary bile acids on the rates of synthesis of all major bile acids was studied in the live rat with an extracorporal bile duct. Bile acid synthesis was determined using HPLC based on mass or by isotope dilution. Derepressed rates of bile acid synthesis (30-54 h) were inhibited by an infusion of taurocholic acid only at a supraphysiological dose of 500 mumol/kg per h, but not at 300 mumol/kg per h, which approximates the initial bile acid secretion (250 mumol/kg per h). When administered together with taurocholic acid (200 mumol/kg per h) only a high dose of taurochenodeoxycholic acid (100 mumol/kg per h) decreased taurocholic but not tauromuricholic or taurochenodeoxycholic acid synthesis. The only bile acid suppressing taurocholic acid (36-71%) and taurochenodeoxycholic acid (up to 33%) formation at an infusion rate close to the normal portal flux was deoxy- or taurodeoxycholic acid at 15-50 mumol/kg per h. It may be concluded that deoxycholic acid and possibly other secondary bile acids are much more potent inhibitors than primary bile acids.

Alanine Transaminase↗

PubMed2005

Conjugated bile acids promote ERK1/2 and AKT activation via a pertussis toxin-sensitive mechanism in murine and human hepatocytes.

Several studies have argued that G-protein-coupled receptors (GPCR) have the capacity to promote activation of receptor tyrosine kinases. The current studies were performed to examine the regulation of the extracellular regulated kinase (ERK)1/2 and AKT pathways by conjugated and unconjugated bile acids in primary hepatocytes. Deoxycholic acid (DCA), chenodeoxycholic acid (CDCA), taurodeoxycholic acid (TDCA), glycodeoxycholic acid (GDCA), taurochenodeoxycholic acid (TCDCA), glycochenodeoxycholic acid (GCDCA), taurocholic acid (TCA), glycocholic acid (GCA), and tauroursodeoxycholic acid (TUDCA) all activated ERK1/2 in primary rat hepatocytes that was abolished by inhibition of ERBB1, and significantly reduced by ROS quenching agents. Bile acid-induced AKT activation was blunted by preventing ERBB1 activation and ROS generation. Treatment of rat hepatocytes with pertussis toxin (PTX) did not alter ERK1/2 and AKT activation induced by DCA or CDCA but abolished pathway activations by conjugated bile acids. Similar data to those with PTX were obtained when a dominant negative form of G(i1alpha) was overexpressed. Treatment of rat hepatocytes with TDCA and TCA promoted guanosine triphosphate (GTP) loading of G(i1alpha), G(i2alpha), and G(i3alpha) in vitro. Treatment of rat hepatocytes with PTX abolished TDCA-induced tyrosine phosphorylation of ERBB1. Similar findings to those in rat hepatocytes were also obtained in primary mouse and human hepatocytes, but not in established rodent or human hepatoma cell lines. In conclusion, collectively our findings demonstrate that unconjugated bile acids activate hepatocyte receptor tyrosine kinases and intracellular signaling pathways in a ROS-dependent manner. In contrast, conjugated bile acids primarily activate receptor tyrosine kinases and intracellular signaling pathways in a GPCR (G(ialpha))-dependent and ROS-dependent manner.

Animals↗

PubMed1993

Mechanism of trichloroethylene-induced elevation of individual serum bile acids. I. Correlation of trichloroethylene concentrations to bile acids in rat serum.

The temporal relationship between trichloroethylene (TRI) and individual serum bile acids (SBA) has been investigated to gain insight into the mechanism of solvent-induced increases in SBA. Male Sprague-Dawley rats were treated with 1 mmol/kg TRI in corn oil, while control rats received only corn oil. Blood samples were collected from the abdominal aorta at 2, 4, 8, and 16 hr after dosing. Individual SBA were determined by high-performance liquid chromatography (HPLC). Liver and blood concentrations of TRI and one of its metabolites, trichloroethanol (TCEOH), were determined by gas chromatography. SBA levels reached their peak at 4 hr and returned to control levels by 16 hr. There was a relationship between SBA levels and TRI concentrations, which were also at their peak 4 hr after dosing. By 16 hr the levels were undetectable. However, peak blood concentrations of TCEOH were reached 8 hr after dosing, and remained high at 16 hr. Cholic acid and taurocholic acid showed the highest levels of bile acids. Some other bile acids were also elevated, including deoxycholic acid, taurodeoxycholic acid, ursodeoxycholic acid, chenodeoxycholic acid, and taurochenodeoxycholic acid. Determination of total bile acids in serum using an enzymatic/colorimetric method showed a similar pattern of response to that obtained with the HPLC analysis. The data are consistent with TRI having a rapid and specific effect on SBA levels by a mechanism other than liver cell damage.

Animals↗

PubMed2003

Quantification of bile acids directly from urine by MALDI-TOF-MS.

The ability to quantify mixtures of bile acids using matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry directly from urine has been demonstrated. Six cholic acid derivatives were selected for analysis: taurocholic acid (TCA), taurochenodeoxycholic acid (TCDCA), taurolithocholic acid (TLCA), glycocholic acid (GCA), glycochenodeoxycholic acid (GCDCA), and glycolithocholic acid (GCDCA). Urine samples were pre-concentrated and purified using solid-phase extraction (SPE) columns. The method was optimized to eliminate suppression effects, and proved to be reproducible from day to day. Calibration curves averaged from three days were obtained for the bile acids directly from urine, and then tested for their ability to accurately determine concentrations from one measurement. In summary, a simple, rapid method has been developed for the quantification of bile salts from urine with SPE clean-up by MALDI-MS.

Bile Acids and Salts↗