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PubMed1988

Lyophilized Clostridium perfringens 3 alpha- and Clostridium bifermentans 7 alpha-hydroxysteroid dehydrogenases: two new stable enzyme preparations for routine bile acid analysis.

Preparations of 3 alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50) from Clostridium perfringens were successfully lyophilized into a stable powder form. Purification of the enzyme was achieved using triazine dye affinity chromatography. C. perfringens 3 alpha-hydroxysteroid dehydrogenase was purified 24-fold using Reactive Red 120 (Procion Red) -cross-linked agarose (70% yield). Quantitative measurement of bile acids with the purified enzymes, 3 alpha-hydroxysteroid dehydrogenase and 7 alpha-hydroxysteroid dehydrogenase (EC 1.1.1.159) from Clostridium bifermentans (strain F-6), was achieved spectrophotometrically. Standard curves with chenodeoxycholic acid (CDC) and cholic acid were linear within a concentration range of 20-100 microM. Analysis of mixtures of ursodeoxycholic acid and CDC showed the additive nature of the 3 alpha-hydroxysteroid dehydrogenase and showed also that 7 alpha-hydroxyl groups were independently quantified by the 7 alpha-hydroxysteroid dehydrogenase. Bile acids in Folch extracts of human bile samples were measured using purified preparations of Pseudomonas testosteroni 3 alpha-hydroxysteroid dehydrogenase, C. perfringens 3 alpha-hydroxysteroid dehydrogenase, Escherichia coli 7 alpha-hydroxysteroid dehydrogenase and C. bifermentans (strain F-6) 7 alpha-hydroxysteroid dehydrogenase. Statistical comparison validated the use of C. perfringens 3 alpha- and C. bifermentans 7 alpha-hydroxysteroid dehydrogenases for the quantification of bile acids in bile.

3-Hydroxysteroid Dehydrogenases↗

PubMed1986

Multicomponent analysis of bile acids in faeces by anion exchange and capillary column gas-liquid chromatography: application in oxytetracycline treated subjects.

A method is described for the multicomponent analysis of bile acids in faeces. Following homogenization and extraction, bile acids are separated into several groups according to their mode of conjugation by anion exchange chromatography on DEAE-Sephadex A-25 in the acetate form. The different conjugate groups are then processed separately and quantified using capillary column gas-liquid chromatography (GC), the identity of the individual bile acid components being established by gas chromatography-mass spectrometry (GC-MS). The method permits the quantitative determination, with good precision, of unconjugated bile acids, their saponifiable derivatives, and their glycine-, taurine- and sulfated conjugates. In five healthy men the mean daily excretion of bile acids was 472 +/- 21.8 mumol (SEM) and the mean faecal concentration 7.74 +/- 1.07 mumol (SEM)/g dry weight. Free bile acids constituted 74.8% +/- 5.8% (SEM), saponifiable conjugates 23.5% +/- 5.8% (SEM) glycine-conjugates 0.7% +/- 0.2% (SEM), taurine-conjugates 0.2% +/- 0.07% (SEM), and their sulfated conjugates 0.8% +/- 0.1% (SEM) of total faecal bile acids. In addition to a detailed description of the methodology the effect of antibiotics on faecal bile acid profiles is presented. Oxytetracycline consistently decreased faecal concentrations of saponifiable derivatives of bile acids while increasing the taurine- and sulfated conjugates. The concentrations of the primary bile acids, cholic- and chenodeoxycholic acid, were higher during the course of oxytetracycline.

Adult↗

PubMed1988

Shark repellent lipophilic constituents in the defense secretion of the Moses sole (Pardachirus marmoratus).

The defense secretion of Moses sole (Pardachirus marmoratus), the fish known to repel sharks, contains lipophilic ichthyotoxins in addition to pardaxin, a peptidic ichthyotoxin. Pardaxin has previously been regarded as the only factor responsible for the shark repellency of the secretion. On the basis of the shark repellent activity observed with the lipophile, it is considered to participate in the repellency of the secretion. Further separation of the toxic lipophile yielded five steroid monoglycosides, named mosesins. Their structures have been elucidated by nuclear magnetic resonance spectroscopy and corroborated by correlating them spectroscopically or chemically to cholic acid or to pavoninins, the related glycosides isolated from the secretion of the congeneric peacock sole, P. pavoninus.

Animals↗

PubMed1986

Effect of petroleum hydrocarbons on the biliary bile acid composition of rainbow trout (Salmo gairdneri).

Biliary bile acid profiles were investigated by thin layer and gas liquid chromatography in fish exposed per os with a Venezuelan crude petroleum or a triglyceride rich oil, olive oil. Neither volume of bile nor bile acid pools were affected, compared to controls, in fish fed either petroleum or olive oil. The response was not uniform, but a small increase in the ratio of the primary bile acids, cholic to chenodeoxycholic, was observed in a number of fish exposed to petroleum. Petroleum appeared not to simply mimic a fatty food source in altering the cholic to chenodeoxycholic acid ratio. The hypothesis that the elevation of mixed function oxygenase enzymes by such potent inducers as petroleum hydrocarbons could markedly alter bile acid profiles, or result in the production of novel bile acid metabolites, was not supported in this study.

Animals↗

PubMed2003

Modeling of preparative chromatography processes with slow intraparticle mass transport kinetics.

Mathematical modeling of the preparative chromatography process accompanied with complex intraparticle mass transport mechanism involving surface diffusion is discussed. As an experimental base for the analysis two steroid compounds, methyl esters of hydroxycholanic acids (bile acids), deoxycholic and cholic acids were selected. For these compounds surface diffusion kinetics were found to have a marked influence on the band broadening. The isocratic chromatography process was performed in a normal-phase preparative system with ternary mixture of solvents containing hexane, ethyl acetate and methanol as a modifier under different operating conditions, e.g., at various mobile phase compositions and inlet concentrations. The efficiency of the system was found to be dependent on the mass of sample injected as well as on the contents of the modifier. Such a phenomenon was suggested to originate from the contribution of the surface diffusion kinetics to the overall mass transport mechanism. For identifying the general trends and concentration dependencies of the surface diffusion coefficient the simplified approach was proposed. The set of chromatographic band profiles registered at different inlet concentration and mobile phase composition were used for determining the influence of the local solid-phase concentration on the mass transport mechanism. For the simulations the transport-dispersive model was used, in which all sources of mass transport resistances were lumped in the properly adjusted mass transport coefficient. The accuracy of this model was verified by comparing its predictions to the solutions of the general rate model.

Chromatography, Liquid↗

PubMed1998

Copper(II) increases bile acid binding to asparagine.

Interactions of two bile acids (cholic and glycocholic acids) with asparagine have been studied by potentiometry in aqueous solutions under conditions similar to those observed in biological fluids (37 degrees C and I = 0.15 M NaCl), and in the absence and presence of copper(II). To characterize the equilibria for the systems copper(II)/bile acid/asparagine, specifically to assess cooperative binding between bile acids and asparagine, the acidity constant of asparagine and formation constants for copper(II)/bile acid and copper(II)/asparagine were also obtained under the same conditions. The results obtained suggest cooperativity in the binding of bile acid to asparagine in the presence of copper(II).

Asparagine↗

PubMed2003

Effect of mdr2 mutation with combined tandem disruption of canalicular glycoprotein transporters by cyclosporine A on bile formation in mice.

UNLABELLED: The inhibition of canalicular glycoprotein transporters has been suggested as the cause of familial intrahepatic cholestasis. Mutations in multidrug resistance 3-glycoprotein (MDR3) gene induce progressive familial intrahepatic cholestasis type 3 (PFIC3). Phenotypically, mutation in mdr2 in mice resembles the disruption of MDR3 in human. Secondly, mutation in the bile salt exporting pump (BSEP)/sister of P-glycoprotein (spgp) gene causes progressive familial intrahepatic cholestasis type 2 in human. However, in spgp knock-out mice only a mild persistent cholestasis occurs. The aim of this study is to evaluate the effects of various P-glycoprotein (Pgp) transporters on bile formation and the canalicular transport of taurocholic acid (TCA) in an attempt to understand the combined role of these transporters in the pathogenesis of familial intrahepatic cholestasis. Total bile acid (TBA) and cholic acid secretion rate were decreased in the mdr2 knock-out mice. However, bile flow (BF) and the secretion of muricholic acids were increased. Secretion of cholesterol was negligible and no phospholipids were detected in bile of mdr2 knock-out mice. Treatment with cyclosporine A (CsA) decreased the BF, and the biliary secretion of bile salts (BS) and phospholipids as compared to wild type mice, but after the injection of TCA+CsA, the BF, and the biliary secretion of BS and lipids were increased as compared to the wild type mice treated with CsA alone. In the mdr2 knock-out mice, CsA treatment decreased the BF and the secretion of BS but after the injection of TCA+CsA, the BF and the biliary secretion of BS were increased and the phospholipid secretion was slightly stimulated as compared to the mdr2 knock-out mice treated with CsA alone. CONCLUSION: Disruption of the mdr2 gene and the inhibition of glycoprotein transporters by CsA induce cholestasis in mice which is characterized by reduced BF, BS and biliary lipid secretion. However, CsA treatment did not significantly increase the cholestatic effect in the mdr2 knock-out mice. The injection of TCA decreased the cholestatic effect in the mdr2 knock-out mice as well as the inhibition of glycoproteins transporters by CsA. These data suggest that mutation in the canalicular mdr2 is an important factor during the development of progressive familial cholestasis.

ATP Binding Cassette Transporter, Subfamily B↗

PubMed1972

Comparative studies of bile salts. A new type of bile salt from Arapaima gigas (Cuvier) (family Osteoglossidae).

1. Arapaima gigas bile salts were hydrolysed by alkali or cleaved with dioxan-trichloroacetic acid to give cholic acid, arapaimic acid, arapaimol-A and arapaimol-B. 2. I.r., n.m.r. and mass spectroscopy and [alpha](D) measurements indicated that arapaimic acid and arapaimol-A and -B are respectively 2alpha,3alpha,7alpha,12alpha-tetrahydroxy-5beta,25in-cholestan-26-oic acid, 5beta,25R-cholestane-2beta,3alpha,7alpha,12alpha,26-pentol and 5beta-cholestane-2beta,3alpha,7alpha,12alpha,26,27-hexol. 3. Partial synthesis of 2beta,3alpha,7alpha,12alpha-tetrahydroxy-5alpha- and -5beta-cholan-24-oic acid and their spectral examination fully confirmed these conclusions. 4. A. gigas bile salts show primitive features in that they comprise alcohol sulphates and a C(27) acid; they are also specialized in showing 2beta-hydroxylation.

Animals↗

PubMed1995

Suppression of sterol 27-hydroxylase mRNA and transcriptional activity by bile acids in cultured rat hepatocytes.

In previous work we have demonstrated suppression of cholesterol 7 alpha-hydroxylase by bile acids at the level of mRNA and transcription, resulting in a similar decline in bile acid synthesis in cultured rat hepatocytes [Twisk, Lehmann and Princen (1993) Biochem. J. 290, 685-691]. In view of the substantial contribution of the 'alternative' or '27-hydroxylase' route to total bile acid synthesis, as demonstrated in cultured rat hepatocytes and in vivo in humans, we here evaluate the effects of various bile acids commonly found in bile of rats on the regulation of sterol 27-hydroxylase in cultured rat hepatocytes. Addition of taurocholic acid, the predominant bile acid in rat bile, to the culture medium of rat hepatocytes resulted in a 72% inhibition of sterol 27-hydroxylase activity. The effect was exerted at the level of sterol 27-hydroxylase mRNA, showing a time- and dose-dependent decline with a maximal suppression (-75%) at 50 microM taurocholic acid after 24 h of culture. The decline in mRNA followed first-order kinetics with an apparent half-life of 13 h. Under these conditions cholesterol 7 alpha-hydroxylase mRNA (-91%) and bile acid synthesis (i.e. chenodeoxycholic and beta-muricholic acid, -81%) were also maximally suppressed. In contrast, no change was found in the level of lithocholic acid 6 beta-hydroxylase mRNA. Assessment of the transcriptional activity of a number of genes involved in routing of cholesterol towards bile acids showed similar suppressive effects of taurocholate on expression of the sterol 27-hydroxylase and cholesterol 7 alpha-hydroxylase genes (-43% and -42% respectively), whereas expression of the lithocholic 6 beta-hydroxylase gene was not affected. Taurocholic acid and unconjugated cholic acid were equally as effective in suppressing sterol 27-hydroxylase mRNA. The more hydrophobic bile acids, chenodeoxycholic acid and deoxycholic acid, also produced a strong inhibition of 57% and 76% respectively, whereas the hydrophilic beta-muricholic acid was not active. We conclude that (1) a number of bile acids, at physiological concentrations, suppress sterol 27-hydroxylase by down-regulation of sterol 27-hydroxylase mRNA and transcriptional activity and (2) co-ordinated suppression of both sterol 27-hydroxylase and cholesterol 7 alpha-hydroxylase results in inhibition of bile acid synthesis in cultured rat hepatocytes.

Adenosine Triphosphate↗

PubMed1987

Fecal steroids and colorectal cancer.

The fecal steroid profiles of healthy subjects were compared with those of colorectal cancer (CRC) patients. The multicomponent profiles did not differ qualitatively in that CRC patients, like control subjects, had similar fecal steroids. The major bile acids detected in fecal extracts were lithocholic acid (LCA) and deoxycholic acid (DCA). The major sterol of animal origin was cholesterol and its bacterial metabolite coprostanol, whereas the major plant sterols were beta-sitosterol, stigmasterol, campesterol, and their corresponding bacterial metabolites. CRC patients excreted higher amounts of total major bile acids (LCA and DCA) than did the control group, but this difference was not significant. However, the LCA-to-DCA ratio was much higher in the CRC group [(1.43, p less than 0.01) compared with the control group (0.72)]. The control group excreted significantly higher amounts of total neutral sterols (p less than 0.001), sterols of animal origin (p less than 0.001), and plant sterols (p less than 0.001) compared with the CRC group; the plant sterols represented a much lower proportion of excreted total neutral sterols in the CRC group (p greater than 0.001) compared with the control group. We propose the following hypotheses. The LCA-to-DCA ratio may be an important discriminant market for CRC susceptibility. The fecal LCA-to-DCA ratio may depend on the differential hepatic synthesis of their respective precursors chenodeoxycholic acid (CDCA) and cholic acid. Hepatic synthesis of CDCA may be increased by more efficient conservation of dietary cholesterol because it has been shown that cholesterol of exogenous origin is the main precursor of this bile acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Acids and Salts↗

PubMed1977

Bile acids, diarrhea, and antibiotics: data, speculation, and a unifying hypothesis.

The primary bile acid, chenodeoxycholic acid, and the secondary bile acid, deoxycholic acid, when present at a concentration of greater than 3 mM, induce salt and water secretion from the human colon and cause a marked increase in the permeability of the human colon to molecules of a molecular weight of 200-500 daltons. Scanning electron microscopy indicates that this action may be associated with tissue damage in some species. In the healthy individual, the primary bile acids, cholic and chenodeoxycholic acid, are dehydroxylated in the colon and are simultaneously precipitated from solution; at pH less than 7, deoxycholic and lithocholic acid are insoluble. In patients with bile acid diarrhea resulting from bile acid malabsorption, dehydroxylation is decreased, and the concentration of bile acids in the colon is markedly elevated. The major secretory bile acid in solution is chenodeoxycholic acid. Administration of cholestyramine, a resin that binds bile acid, reduces the elevated concentration of chenodeoxycholic acid and abolishes the diarrhea. These facts can be used to develop a unifying hypothesis which proposes that elevated concentrations of primary bile acids in the colon play a role in diarrhea and pseudomembranous colitis induced by clindamycin.

Anti-Bacterial Agents↗

PubMed1994

Effects of bile salt and phospholipid hydrophobicity on lithogenicity of human gallbladder bile.

Increased biliary bile salt and phospholipid hydrophobicity may promote nucleation of cholesterol crystals and gallstone formation. We therefore compared bile salt composition (determined by gas-liquid chromatography) in patients with cholesterol (n = 35) and pigment (n = 16) gallstones (group A). Bile salt composition and cumulative bile salt hydrophobicity index were not different between both stone types. Hydrophobicity index or % of individual bile salts did not correlate with cholesterol saturation index or nucleation time. In an additional 21 cholesterol stone patients (group B) biliary bile salt and phospholipid hydrophobicity as determined by high-pressure liquid chromatography did not correlate with cholesterol saturation index or nucleation time. In both group A and group B, cholesterol stone patients with cholesterol crystals in their fresh biles had a higher % deoxycholic acid, a lower % cholic acid and a higher bile salt hydrophobicity index than crystal-negative patients. This study indicates the need for further research on the role of bile salt hydrophobicity in the pathogenesis of gallstones.

Adult↗

PubMed1998

Bile acids influence hepatic chemiluminescence in normal and oxidative-stressed rats.

The aim of the present study was to clarify whether bile acids influence chemiluminescence (CL) in the liver in vivo. Hepatic CL was determined on the surface of the liver of anaesthetized rats by using a photon counter. In normal rats, hepatic CL was significantly decreased 30 min after enteral administration of chenodeoxycholic acid (CDCA) or deoxycholic acid (DCA), but returned to its initial level 3 h later, after part of the CDCA administered was metabolized. Ursodeoxycholic acid (UDCA) and cholic acid had no effect on CL. In contrast, hepatic CL was markedly increased 30 min after CDCA or DCA administration in rats given either buthionine sulphoximine (BSO), an inhibitor of gamma-glutamylcysteine synthetase, or diethyldithiocarbamate (DDC), an inhibitor of both superoxide dismutase and glutathione peroxidase. Chenodeoxycholic acid further increased the CL of BSO- or DDC-treated rats during inhalation of oxygen via a tracheal cannula. Coadministration of UDCA eliminated the effects of CDCA on the hepatic CL of normal and BSO- or DDC-treated rats with or without oxygen inhalation. We conclude that cytotoxic bile acids, such as CDCA, increase CL in the antioxidants-depleted or oxidative-stressed liver in vivo, but that UDCA prevents CDCA from developing CL.

Animals↗

PubMedDate not supplied

Acute and reversible fatty metamorphosis of cultured rat hepatocytes.

Rat hepatocyte cell line M6, B347 and J525, among which only M6 is slightly deviated from diploidy, showed marked microvesicular fatty metamorphosis in response to treatment with Tweens at concentrations of 0.05-0.025% in Eagle's minimum essential medium (MEM). Within 24 h treated cells became fatty at 100% in frequency and filled with small lipid droplets, as revealed by fat staining or at the ultrastructural level. Fatty hepatocytes, however, took again non-fatty morphology 72 h after withdrawal of Tweens from the culture medium. Growth of the cell exhibited mild retardation at the early phase of the treatment but almost similar cell density to that of control cells was achieved 24 h after the treatment. Other detergents without fatty-acid moiety, including NP-40, triton X-100, sodium deoxycholic acid and sodium cholic acid, were ineffective to induce fatty change. Oleate, a fatty-acid moiety of Tween 80 or 85, and linolate caused reversible fatty metamorphosis of the cell lines at concentrations of 1.9 x 10(4) mol/L or more and 3.8 x 10(4) mol/L or more, respectively. Ethanol induced mild steatosis of the cell lines and enhanced fatty change by linolate. Hepatic fatty acid-binding protein was not detected in the cell lines before or after the induction of fatty change. These results indicate that fatty acid itself is directly incorporated in cultured rat hepatocytes and expelled 3 days later without apparent cell degeneration.

Animals↗

PubMed1976

Evidence for the absorption of bile acids in the proximal small intestine of normo- and hyperlipidaemic subjects.

Bile acid composition was determined in duodenal and jejunal aspirates obtained under fasting conditions in normolipidaemic controls and in patients with the type IIa and type IV lipoprotein patterns. In 17 out of the 22 subjects studied, the duodenal as compared with the jejunal aspirates contained proportionally more CD (chenodeoxycholic acid) than C (cholic acid). The two types of aspirates also differed slightly with regard to the D (deoxycholic acid): CD ratio, which was higher in samples drawn from the jejunum. These findings, compatible with an absorpiton of about 30% of CD in the upper small intestine, were approximately the same in all groups of patients. As evidenced by additional experiments in two subjects, an oral intake of cream does not significantly influence the absorption of CD in the upper small intestine.

Bile Acids and Salts↗

PubMed1992

Faecal unconjugated bile acids in patients with colorectal cancer or polyps.

The unconjugated faecal bile acid profiles of 14 patients with colorectal cancer, nine patients with polyps and 10 controls were compared using gas liquid chromatography, controlling for such confounding variables as cholecystectomy, gall stones and hepatic function. Patients with adenomatous polyps had a higher concentration of faecal bile acids (5.23 mumol/g, 2.16-13.67 (median, range) v 1.96, 0.91-6.97; p = 0.016) lithocholic acid (2.41, 0.88-3.22 v 1.07, 0.38-2.03; p = 0.013) and total secondary bile acids (5.23, 2.16-13.4 v 1.96, 0.73-6.63; p = 0.02) compared with control subjects. Patients with colorectal cancer had an increased (p = 0.029) proportion of secondary faecal bile acids (mol%) compared with controls (100, 96.5-100 v 95.19, 81.73-100) and the ratios of the primary bile acids, cholic and chenodeoxycholic acid, to their respective derivatives (secondary bile acids) were significantly lower in cancer patients compared with control and patients with polyps (p = 0.034 to 0.004). This study lends further support to the theory that bile acids may play a role in the development of polyps and colorectal cancer.

Adenocarcinoma↗

PubMed1991

Possible mechanism for the cocarcinogenic effect of bile acids: increased intracellular uptake of methylcholanthrene by C3H/10T1/2 fibroblasts in vitro.

The cocarcinogenic effect of bile acids on the chemical transformation of C3H/10T1/2 fibroblasts was examined in vitro. The assimilation of 3H-methylcholanthrene (3H-MCA) by C3H/10T1/2 cells pretreated with bile acids was examined by the measurement of uptake and by autoradiography. Cells that were pretreated for 48 h with bile acids (100 microM lithocholic acid, 500 microM cholic acid) and then maintained in medium that contained 3H-MCA showed an increase in radioactivity compared to control cells. These results indicate that the transfer of carcinogens into cells is enhanced by pretreatment with bile acids.

Animals↗

PubMed1972

The formation of abnormal bile and cholesterol gallstones from dietary cholesterol in the prairie dog.

To study the pathogenesis of cholesterol gallstones, we fed 24 adult male prairie dogs a high cholesterol, egg yolk diet. 13 control animals received a cholesterol-free diet. All animals fed the egg yolk diet formed multiple gallstones in 2-6 months' time. These stones contained cholesterol, 77+/-14% by dry weight. No stones ocurred in the control group. The egg yolk-fed animals developed bile of altered chemical composition. The cholesterol concentration of hepatic and gallbladder bile increased significantly. The molar ratios of bile acid/cholesterol and phospholipid/cholesterol decreased in hepatic and gallbladder bile. The predominant bile acid shifted from cholic acid, 78% of the total bile acids, to chenodeoxycholic acid, 60% of the total. In common bile duct cannulated animals the high cholesterol diet produced increased secretion of cholesterol by the liver and increased bile flow. In animals fed the egg yolk diet for 2 months, cholesterol-4-(14)C was included in the daily diet for the next 4 months to establish an isotopic steady state. At autopsy the mean specific activity of cholesterol was similar in serum, liver, hepatic bile, gallbladder bile, and gallstones. Thus the cholesterol of gallstones apparently equilibrated constantly throughout the study and was not sequestrated as a static pool. The high cholesterol, egg yolk diet caused the secretion of an "abnormal bile" which led to precipitation of cholesterol from micellar solution. The increased bile cholesterol relative to bile acid and phospholipid favored stone formation. This dietary induction of cholesterol gallstones provided a unique animal model, in part but not completely analogous to human cholelithiasis.

Animals↗