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PubMed1976

Preparation of the 3-monosulphates of cholic acid, chenodeoxycholic acid and deoxycholic acid.

1. The 3-sulphates of cholic, chenodeoxycholic and deoxycholic acids were prepared as crystalline disodium salts. 2. The method described shows that it is possible to prepare specific sulphate esters of polyhydroxy bile acids and to remove protecting acyl groups without removing the sulphate. 3. A study of bile acid sulphate solvolysis showed that none of the usual methods give the original bile acid in major yield in a single step. 4. An understanding of the preparation, properties and methods of solvolysis of bile acid sulphates is basic for investigations of cholestasis and liver disease.

Acetylation↗
PubMed1992

Comparative hepatotoxicity of cholic acid, deoxycholic acid and lithocholic acid in the rat: in vivo and in vitro studies.

Until now, the cytotoxicity of the bile acids was mostly seen as being inversely associated with their degree of lipophilicity. The present study aimed at comparing the hepatotoxicity of cholic acid (CA), deoxycholic acid (DCA) and lithocholic acid (LCA), which are respectively, tri-, di- and monohydroxylated bile acids. For in vivo studies, the bile acids have been given at the dose of 0.5% or 1% in the diet of male Wistar rats for 2 weeks. The histological analysis of the liver, and the measurement of serum parameters of cytotoxicity and cholestasis (aminotransferases activity, bilirubin and total bile acids concentration), indicate that, among the bile acids tested, DCA is the most hepatotoxic, at both doses, while CA is the least hepatotoxic and cholestatic compound. Moreover, DCA is the only bile acid which, when given at the dose of 0.5%, induces lipid peroxidation in the liver, as evidenced by the measurement of thiobarbituric reactive substances in liver homogenates. The analysis of bile acids in liver homogenates by gas liquid chromatography revealed that feeding the animals with DCA results in its hepatic accumulation. Feeding rats with LCA or CA only slightly modifies the proportion of tri-, di- and monohydroxylated bile acids in the liver, as compared to controls. An in vitro experiment aimed at studying the hepatocellular lysis induced in vitro by the three bile acids by measuring the release of lactate dehydrogenase in the incubation medium of surviving hepatocytes in suspension. At a concentration of 1 mM, only DCA induces a significant cellular lysis, while at this concentration the lytic effects of CA and LCA are progressive and time-dependent. From this study, we gather that the hepatotoxicity of bile acids does not necessarily depend on their degree of hydroxylation. Our results are in accordance with some studies in rat hepatocarcinogenesis, showing a predominant initiating and promoting effects of DCA, as compared to LCA.

Administration, Oral↗
PubMed1979

Measurement of cholic acid synthesis and secretion by isolated rat hepatocytes.

Liver cells isolated from normal and cholestyramine-treated rats were incubated as cell suspensions for up to 4 hr in a simple, defined medium. The bile acid concentration in cells plus cell medium was determined by gas-liquid chromatography. Normal hepatocytes synthesized cholic acid at an initial rate of 0.25 nmol/mg cell protein per hr, which is comparable to rates reported from in vivo methods. This rate was increased more than 4-fold when rats were fed a cholestyramine-containing diet for 7 days prior to liver cell isolation. Although cholic acid was secreted into the cell medium during the incubation, it could not be assayed reliably by the hydroxysteroid dehydrogenase assay method, contrary to the reports of Anwer et al. 1975. Biochem. Biophys. Res. Commun. 64: 603 and Gardner and Chenouda 1978. J. Lipid Res. 19: 985.

Animals↗
PubMedDate not supplied

[Characteristics of a Mycobacterium mucosum culture oxidizing cholic acid].

Some physiologo-morphological and biochemical characteristics were studied with the culture of Mycobacterium mucosum 1210 which can assimilate cholic acid as a sole source of carbon. This culture is capable of spontaneous variability. Four variants of the culture were obtained which possessed different rates of the transformation of cholic acid. The variant which formed slimy colonies of pale-yellow colour was the most active. Some morphological modifications of the cells were investigated in the course of cultivation, such as the size, shape and formation of the capsules. Various growth media were tested, and the optimal values of pH were selected.

Cell-Free System↗
PubMed1976

Effects of a fat-reduced diet on the faecal excretion of radioactivity following administration of 14C-cholic acid and on the duodenal concentration of bile salts in patients with ileal disease.

The fraction of faecal radioactivity excreted after intravenous administration of 14C-labelled cholic acid decreased in most patients with ileopathy and bile salt malabsorption when the dietary daily fat content was reduced from 100 to 40 g. The decreased faecal cholic acid loss might be due to increased bile salt absorption and decreased emptying of the gall-bladder on the fat-reduced diet. A simplified method to determine the corrected 24-hour excretion of radiologically labelled bile salts is described.

Adult↗
PubMed1980

Effect of dietary cholic acid and cholesterol on liver and kidney cystathionase and cysteine sulfinate decarboxylase activities and taurine concentrations in the rat.

Hepatic cystathionase and cysteine sulfinate decarboxylase activities are drastically affected by cholic acid added to the diet without cholesterol. When cholic acid and cholesterol are given together, only cysteine sulfinate decarboxylase activity is changed. Neither kidney enzyme activity nor taurine concentrations in the liver and kidney are noticeably modified, whatever the diet.

Animals↗
PubMed1982

The influence of cholic acid and cholesterol on cell proliferation in the gallbladder mucosa of the mouse.

The effect of a cholesterol-cholic acid diet on cell proliferation in the gallbladder epithelial cells of the mouse was investigated systematically. As early as 48 h after the commencement of the diet an outburst of proliferative activity in the gallbladder epithelium was observed. This accelerated proliferation was accompanied by an increased exfoliation of epithelial cells into the gallbladder lumen. In the further course of the experimental diet the 3H-labelling index fell but remained significantly higher than in the control group. The epithelium displayed villus-like folds, and the gallbladder wall became noticeably thicker. The cholesterol-cholic acid diet stimulated proliferation not only in the gallbladder epithelial cells but also in fibroblasts and hepatocytes.

Animals↗
PubMed1979

7alpha-Dehydroxylation of cholic acid and chenodeoxycholic acid by Clostridium leptum.

The rate of 7alpha-dehydroxylation of primary bile acids was quantitatively measured radiochromatographically in anaerobically washed whole cell suspensions of Clostridium leptum. The pH optimum for the 7alpha-dehydroxylation of both cholic and chenodeoxycholic acid was 6.5-7.0. Substrate saturation curves were observed for the 7alpha-dehydroxylation of cholic and chenodeoxycholic acid. However, cholic acid whole cell K0.5 (0.37 micron) and V (0.20 mumol hr-1mg protein-1) values differed significantly from chenodeoxycholic acid whole cell K0.5 (0.18 micron) and V (0.50 mumol-1 hr-1 mg protein-1). 7alpha-Dehydroxylation activity was not detected using glycine and taurine-conjugated primary bile acids, ursodeoxycholic acid, cholic acid methyl ester, or hyocholic acid as substrates. Substrate competition experiments showed that cholic acid 7 alpha-dehydroxylation was reduced by increasing concentrations of chendeoxycholic acid; however, chenodeoxycholic acid 7alpha-dehydroxylation activity was unaffected by increasing concentrations of cholic acid. A 10-fold increase in cholic and 7alpha-dehydroxylation activity occurred during the transition from logarithmic to stationary phase growth whether cells were cultured in the presence or absence of sodium cholate. In the same culture, a similar increase in chenodeoxycholic acid 7alpha-dehydroxylation was detected only in cells cultured in the presence of sodium cholate. These results indicate the possible existence of two independent systems for 7alpha-dehydroxylation in C. Leptum.

Chenodeoxycholic Acid↗
PubMed1984

Drug-binding properties of rat alpha 1-foetoprotein. Binding of warfarin, phenylbutazone, azapropazone, diazepam, digitoxin and cholic acid.

As part of an investigation into whether alpha 1-foetoprotein (alpha 1-FP) plays the same transport role in foetal serum as albumin does in the adult, the binding properties of both proteins were compared with respect to the binding of a series of compounds known to be bound by albumin's specific drug-binding sites. The binding of warfarin, phenylbutazone, azapropazone, diazepam, digitoxin and cholic acid by rat alpha 1-FP and serum albumin was studied by equilibrium dialysis at 4 degrees C. Rat alpha 1-FP was shown to have neither albumin's high-affinity site II (diazepam as marker) nor its site III (digitoxin and cholic acid as markers). High-affinity binding by alpha 1-FP was found for the specific markers (warfarin, phenylbutazone, azapropazone) of albumin's drug-binding site I. However, instead of albumin's one high-affinity site/molecule, a mean value of 0.5 site/molecule was obtained with rat alpha 1-FP. Charcoal treatment at neutral pH of rat serum albumin did not affect its measured binding properties, but treatment of the alpha 1-FP led to an increased affinity for warfarin, phenylbutazone and azapropazone without a change in the measured number of sites, indicating competition for binding at this site by (an) endogenous ligand(s). These results are discussed in terms of the structures of the two proteins and with respect to the physiological implications of the differences found.

Animals↗
PubMed1990

[Bacteriocholia and cholic acid level in the bile in cholelithiasis].

Infection of the biliferous system in patients with cholelithiasis was shown to be the most frequent when the levels of cholic acid in bile were low. Physiological concentrations of cholic and deoxycholic acids have antimicrobial activity against organisms not adapted to the presence in bile. Outer drainage of the bile ducts was accompanied by an increase in the levels of cholic acid when at the background of outer decompression bacteria were eliminated from the biliferous system. In vitro studies revealed a synergistic antibacterial effect of cholic and deoxycholic acid combinations with cefazolin.

Bile↗
PubMedDate not supplied

[Antibacterial activity of the derivatives of cholic acid (author's transl)].

The synthesis of derivatives of cholic acid with L-lysine and Lysil-lysine with antibacterial activity, is here described. Derivatives with one molecule of lysine show antibacterial activity at 100 mug/ml concentration, while lysil-lysine derivatives, particularly Col-Lys-Lys-NH2-2HCl, are effective also at 25 mug/ml.

Bacteria↗
PubMed2000

Regulation of 25- and 27-hydroxylation side chain cleavage pathways for cholic acid biosynthesis in humans, rabbits, and mice. Assay of enzyme activities by high-resolution gas chromatography;-mass spectrometry.

In classic cholic acid biosynthesis, a series of ring modifications of cholesterol precede side chain cleavage and yield 5beta-cholestane-3alpha, 7alpha, 12alpha-triol. Side chain reactions of the triol then proceed either by the mitochondrial 27-hydroxylation pathway or by the microsomal 25-hydroxylation pathway. We have developed specific and precise assay methods to measure the activities of key enzymes in both pathways, 5beta-cholestane-3alpha, 7alpha, 12alpha-triol 25- and 27-hydroxylases and 5beta-cholestane-3alpha, 7alpha, 12alpha, 25-tetrol 23R-, 24R-, 24S- and 27-hydroxylases. The extracts from either the mitochondrial or microsomal incubation mixtures were purified by means of a disposable silica cartridge column, derivatized into trimethylsilyl ethers, and quantified by gas chromatography;-mass spectrometry with selected-ion monitoring in a high resolution mode. Compared with the addition of substrates in acetone, those in 2-hydroxypropyl-beta-cyclodextrin increased mitochondrial triol 27-hydroxylase activity 132% but decreased activities of the enzymes in microsomal 25-hydroxylation pathway (triol 25-hydroxylase and 5beta-cholestane-3alpha, 7alpha, 12alpha, 25-tetrol 23R-, 24R-, 24S- and 27-hydroxylases) 13;-60% in human liver. The enzyme activities in both pathways were generally 2- to 4-times higher in mouse and rabbit livers compared with human liver. In all species, microsomal triol 25-hydroxylase activities were 4- to 11-times larger than mitochondrial triol 27-hydroxylase activities but the activities of tetrol 24S-hydroxylase were similar to triol 27-hydroxylase activities in our assay conditions. The regulation of both pathways in rabbit liver was studied after bile acid synthesis was perturbed. Cholesterol feeding up-regulated enzyme activities involved in both 25- (64;-142%) and 27- (77%) hydroxylation pathways, while bile drainage up-regulated only the enzymes in the 25-hydroxylation pathway (178;-371%). Using these new assays, we demonstrated that the 25- and 27-hydroxylation pathways for cholic acid biosynthesis are more active in mouse and rabbit than human livers and are separately regulated in rabbit liver.

Animals↗
PubMed2000

Bile acid synthesis in cultured human hepatocytes: support for an alternative biosynthetic pathway to cholic acid.

The biosynthesis of bile acids by primary cultures of normal human hepatocytes has been investigated. A general and sensitive method for the isolation and analysis of sterols and bile acids was used, based on anion exchange chromatography and gas chromatography-mass spectrometry (GC/MS). Following incubation for 5 days, 8 oxysterols and 8 C(27)- or C(24)-bile acids were identified in media and cells. Cholic and chenodeoxycholic acids conjugated with glycine or taurine were by far the major steroids found, accounting for 70% and 24% of the total, respectively, being consistent with bile acid synthesis in human liver. Small amounts of sulfated 3beta-hydroxy-5-cholenoic acid and 3beta,7alpha-dihydroxy-5beta-cholanoic acid were also detected. Nine steroids were potential bile acid precursors (2% of total), the major precursors being 7alpha, 12alpha-dihydroxy-3-oxo-4-cholenoic acid and its 5beta-reduced form. These 2 and 5 other intermediates formed a complete metabolic sequence from cholesterol to cholic acid (CA). This starts with 7alpha-hydroxylation of cholesterol, followed by oxidation to 7alpha-hydroxy-4-cholesten-3-one and 12alpha-hydroxylation. Notably, 27-hydroxylation of the product 7alpha, 12alpha-dihydroxy-4-cholesten-3-one and further oxidation and cleavage of the side chain precede A-ring reduction. A-Ring reduction may also occur before side-chain cleavage, but after 27-hydroxylation, yielding 3alpha,7alpha, 12alpha-trihydroxy-5beta-cholestanoic acid as an intermediate. The amounts of the intermediates increased in parallel to those of CA during 4 days of incubation. Suppressing 27-hydroxylation with cyclosporin A (CsA) resulted in a 10-fold accumulation of 7alpha, 12alpha-dihydroxy-4-cholesten-3-one and a decrease of the production of CA and its acidic precursors. These results suggest that the observed intermediates reflect an alternative biosynthetic pathway to CA, which may be quantitatively significant in the cells.

Bile Acids and Salts↗
PubMed1989

Is cholic acid responsible for embryo-toxicity of the post-receptive uterine environment?

HPLC analysis of the embryo-toxic fraction of human uterine fluid, collected between the 22nd and 25th days of the menstrual cycle, revealed the presence of cholic acid at high concentrations. It is suggested that cholic acid could be responsible for the embryo-toxicity of the uterine environment, which follows the receptive period for implantation.

Cholic Acids↗
PubMed2006

Critical role of cholic acid for development of hypercholesterolemia and gallstones in diabetic mice.

We studied bile acid and cholesterol metabolism in insulin-dependent diabetes utilizing genetically modified mice unable to synthesize cholic acid (Cyp8b1-/-). Diabetes was induced in Cyp8b1-/- and wild type animals (Cyp8b1+/+) by alloxan, and the mice were fed normal or cholesterol-enriched diet for 10 weeks. The serum levels of cholesterol were strongly increased in diabetic Cyp8b1+/+ mice fed cholesterol, while diabetic Cyp8b1-/- mice did not show any aberrations regardless of the diet. Diabetic cholesterol-fed Cyp8b1+/+ mice had much higher biliary cholesterol and cholesterol saturation index than all other groups, their bile contained a large number of cholesterol crystals, and their canalicular cholesterol transporter Abcg5/g8 mRNA levels were much higher. Cyp7a1 mRNA levels were similar in all diabetic mice but higher compared to non-diabetic animals. The results indicate a critical role for cholic acid for the development of hypercholesterolemia and gallstones in our animal model.

Alloxan↗
PubMedDate not supplied

A catecholic 9,10-seco steroid as a product of aerobic catabolism of cholic acid by a Pseudomonas sp.

A mutant of the efficient bile acid-utilizing Pseudomonas putida ATCC 31752 was found to accumulate three major catabolites on aerobic growth on cholic acid. One of these catabolites was isolated and identified as 3,4,7,12 beta-tetrahydroxy-9,10-seco-1,3,5(10)-androstatriene-9,17-dione (2). This is the first catecholic 9,10-secosteroid isolated from the microbial degradation of bile acids or sterols and confirms the role of such secosteroids in the microbial degradative pathway for steroids.

Aerobiosis↗