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Results for “CHOLIC ACID”

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PubMed1983

Cholic acid conjugation test and quantitative liver function in acute liver failure.

In 33 patients with acute hepatic encephalopathy due to toxic or viral hepatitis the following analyses were performed: (24-14C)cholic acid conjugation and sulfation, plasma phenazone clearance, galactose elimination capacity, and concentrations of glycocholic acid and glycolithocholic acid sulfate in plasma. The (24-14C)cholic acid conjugation in patients with viral hepatitis was significantly lower in fatal cases than in patients who survived (p less than 0.002). In these patients the galactose elimination capacity and the plasma phenazone clearance were insignificantly lower. Tauro-(24-14C)cholic acid was the predominant metabolite of (24-14C)cholic acid in six patients, but in four patients with toxic hepatitis this metabolite was only found in trace amounts. Sulfation after 3 h of (24-14C)cholic acid accounted for 0-8.2% of the administered dose. The sulfate of glycolithocholic acid was found in the plasma of all patients. No survival limit with regard to the capacity for the (24-14C)cholic acid conjugation could be defined.

Acute Disease↗

PubMed1976

Kinetics of [14C]cholic acid in fulminant hepatic failure: a prognostic test.

The kinetics of intravenously injected [14C]cholic acid have been investigated in 14 patients with fulminant hepatic failure, 24 to 36 hr after the development of grade IV encephalopathy. Radioactivity was measured in plasma samples and in the individual plasma bile acid fractions after separation by thin layer chromatography. Plasma disappearance curves of the free [14C]cholic acid were calculated by an iterative nonlinear least squares fitting procedure using a computer. The disappearance of total plasma radioactivity was similar in all patients and greatly prolonged compared with healthy subjects. However, the plasma disappearance of free [14C]cholic acid was significantly faster in the 8 patients who recovered consciousness than in the 6 who did not. Plasma disappearance of free [14C]cholic acid correlated highly significantly with the proportion of conjugated [14C]cholate in plasma. All patients in whom more than 70% of plasma radioactivity was in the conjugated fraction 3 hr after injection survived and left hospital, whereas all of those in whom less than 55% was conjugated died. Measuring the percentage conjugation of [14C]cholate 3 hr after injection may therefore be a useful test of residual liver function in hepatic failure, as a guide to prognosis and in evaluating new forms of treatment.

Adolescent↗

PubMed1993

Spermicidal and antiviral properties of cholic acid: contraceptive efficacy of a new vaginal sponge (Protectaid) containing sodium cholate.

Cholic acid (sodium cholate) exhibits a strong spermicidal and antiviral [anti-human immunodeficiency virus (HIV)-1] activity. The same effects are observed for F-5 Gel, the active mixture of a new contraceptive sponge (Protectaid), which contains sodium cholate in association with low concentrations (0.5%) of nonoxynol-9 and benzalkonium chloride. Both cholic acid and the F-5 Gel exert a dose-dependent, in-vitro inhibitory effect (i) on the activity of HIV-1 associated reverse transcriptase in an acellular system and (ii) on the potential of HIV-1 efficiently to infect human lymphocytes. During 12 months use, the contraceptive efficacy of the 'Protectaid' sponge was 100% in 20 young women who had chosen this method for reasons of both contraception and anti-sexually transmitted disease. No side-effects were recorded throughout this period. Cervical cultures at 6-month intervals showed the presence of Mycoplasma hominis and Candida albicans in one or two cases. The combined spermicidal and anti-HIV properties of cholic acid reported in this paper and used in the 'Protectaid' sponge offer a new and modern protective method of contraception.

Adult↗

PubMed1999

Cholic acid aids absorption, biliary secretion, and phase transitions of cholesterol in murine cholelithogenesis.

Cholic acid is a critical component of the lithogenic diet in mice. To determine its pathogenetic roles, we fed chow or 1% cholesterol with or without 0.5% cholic acid to C57L/J male mice, which because of lith genes have 100% gallstone prevalence rates. After 1 yr on the diets, we measured bile flow, biliary lipid secretion rates, hepatic cholesterol and bile salt synthesis, and intestinal cholesterol absorption. After hepatic conjugation with taurine, cholate replaced most tauro-beta-muricholate in bile. Dietary cholic acid plus cholesterol increased bile flow and biliary lipid secretion rates and reduced cholesterol 7alpha-hydroxylase activity significantly mostly via deoxycholic acid, cholate's bacterial 7alpha-dehydroxylation product but did not downregulate cholesterol biosynthesis. Intestinal cholesterol absorption doubled, and biliary cholesterol crystallized as phase boundaries shifted. Feeding mice 1% cholesterol alone produced no lithogenic or homeostatic effects. We conclude that in mice cholic acid promotes biliary cholesterol hypersecretion and cholelithogenesis by enhancing intestinal absorption, hepatic bioavailability, and phase separation of cholesterol in bile.

Absorption↗

PubMed2002

Cholestatic effect of large bilirubin loads and cholestasis protection conferred by cholic acid co-infusion: a molecular and ultrastructural study.

BACKGROUND: Large intravenous bilirubin loads block biliary phospholipid secretion, produce canalicular membrane lesions and cause canalicular cholestasis. Cholic acid co-infusion forestalls these untoward effects. The aim of this study was first to determine whether bilirubin overload causes cholestasis through reducing the activity or the hepatic expression of the bile salt export pump (bsep) or Na-taurocholate co-transporting polypeptide (ntcp) and, secondly, whether cholic acid co-infusion forestalls cholestasis by upregulating bsep, ntcp or phosphoglycoprotein 3 (pgp3) expressions or activities. A further aim was to determine whether large bilirubin infusions also produce ultrastructural changes inside hepatocytes. METHODS: The effects of intravenous infusion of 2 g bilirubin over 150 min on hepatic expression of bsep, ntcp and pgp3 were studied in bile acid-depleted and cholic acid co-infused pigs, and related to canalicular bile acid transport and bile secretion. Effects on hepatocyte ultrastructural morphology were analysed by electron microscopy. RESULTS: Bilirubin-induced cholestasis reflected marked diminution of bsep and pgp3 transport activities and not reduced hepatic expression of these transporters. Hepatocyte ultrastructural abnormalities were predominantly confined to the hepatocyte canalicular membrane in cholestatic livers. Cholic acid co-infusion with bilirubin conferred complete cholestasis protection through enhancing pgp3 and bsep transporter activities and not through upregulating their expression. Bilirubin infusion did not change ntcp expression. CONCLUSION: Bilirubin-induced cholestasis is due to markedly impaired activity of the membrane-embedded bsep transporter consequent upon ultrastructural injury to the canalicular membrane. Cholic acid co-infusion with bilirubin enhances bsep and pgp3 activities and confers protection against canalicular membrane injury and bilirubin-induced cholestasis.

ATP Binding Cassette Transporter, Subfamily B↗

PubMedDate not supplied

[Plasma clearance of cholic acid in patients with chronic diseases of the liver].

The diagnostic value of 14C-cholic acid plasma clearance following oral administration was evaluated. 14C-cholic acid clearance was 1223 +/- 267 mL/min. per 1 square meter in the control group without liver disease. Significantly lower values (p less than 0.001) were obtained in the patients with chronic hepatitis (694 +/- 137 mL/min. per 1 square meter) and liver cirrhosis (332 +/- 156 mL/min. per 1 square meter). Sensitivity of the 14C-cholic acid clearance test was 100% while specificity--80%. A 3-year follow-up has shown that this test is of high prognostic value in patients with liver cirrhosis.

Adult↗

PubMed1992

Comparison of the proportion of unconjugated to total serum cholic acid and the [14C]-xylose breath test in patients with suspected small intestinal bacterial overgrowth.

The proportion of unconjugated to total cholic acid in fasting serum and the 1-gram [14C]-xylose breath test were determined in 36 patients with suspected bacterial overgrowth of the small intestine. Twenty-two patients had an abnormal [14C]-xylose breath test, indicating bacterial overgrowth. The proportion of unconjugated to total cholic acid was significantly higher in the patients with an abnormal breath test compared with those displaying a normal breath test (47 +/- 5% vs 16 +/- 3%). A good correlation was obtained between the proportion of unconjugated to total cholic acid and the breath test (r = 0.63, n = 36). Provided the [14C]-xylose breath test is reliable as a test of bacterial overgrowth, determination of the proportion of unconjugated to total cholic acid in fasting serum had a sensitivity of 73% and a specificity of 94%. It is suggested that determination of the proportion of unconjugated to total cholic acid in peripheral venous blood may be useful as a simple screening test for detection of bacterial contamination of the upper small intestine provided the patients do not have bile acid malabsorption.

Adult↗

PubMed2000

Anionic facial amphiphiles from cholic acid.

[structure:see text] Anionic facial amphiphiles have been prepared from cholic acid. These compounds offer antipodes of recently reported cationic amphiphiles derived from cholic acid. The synthesis of the anionic amphiphiles was accomplished in few steps from a common intermediate. In contrast to many other anionic facial amphiphiles, the cholic acid derived amphiphiles appeared to aggregate at relatively low concentration.

Cholic Acid↗

PubMedDate not supplied

Cholic acid and the heart: in vitro studies of the effect on heart rate and myocardial contractility in the rat.

1. Cholic acid has a dose-dependent negative chronotropic effect on isolated atria of Wistar rats. 2. The positive inotropic effect of cholic acid is the result of a negative chronotropic effect and can be eliminated by electrical pacing. 3. Cholic acid does not appear to exert its negative chronotropic effect through cholinoceptors and alterations in bath concentrations of calcium and potassium does not influence this effect significantly. 4. Cholic acid is a functional antagonist of isoprenaline. 5. It is suggested that cholic acid exerts its negative chronotropic effect by forming a monolayer on the surface of the cell membrane, thereby mechanically interfering with membrane function.

Animals↗

PubMed1993

Induction of peroxisomal beta-oxidation by a microbial catabolite of cholic acid in rat liver and cultured rat hepatocytes.

The capability of (4R)-4-(2,3,4,6,6a beta,7,8,9,9a alpha,9b beta-decahydro-6a beta-methyl-3-oxo-1H-cyclopental[f]quinolin-7 beta-yl)valeric acid (DCQVA), a catabolite of cholic acid produced by enterobacteria, to induce peroxisome proliferation in vivo and in vitro was studied. Rats given 0.3% DCQVA in the diet for 2 weeks showed marked increases in peroxisomal beta-oxidation, mitochondrial 2,4-dienoyl-CoA reductase and microsomal laurate omega-oxidation activities in the liver compared with control rats given the diet without DCQVA. Cultured rat hepatocytes treated with DCQVA for 72 h also exhibited greatly enhanced beta-oxidation activity. The increased activity was concentration-dependent and the effective concentrations were comparable with those of clofibric acid that produced the same degree of induction in the assay. The results demonstrate that DCQVA is a potent peroxisome proliferator that occurs naturally in rat intestine.

Animals↗

PubMed1979

Cholic acid accumulation by the ciliary body and by the iris of the primate eye.

Cholic acid accumulates in both the ciliary body and the iris of the primate eye during in vitro incubations at 37 degrees C for 1 hr. Incubation at 0 degrees C depresses uptake in both tissues. The washout of preaccumulated cholic acid occurs some 3.4 times faster from the iris than from the ciliary body. The mechanism of cholic acid accumulation in both tissues is less sensitive to inhibition by high iodipamide concentrations and also is less sensitive to inhibition by high hippurate concentrations than the mechanism of p-aminohippurate (PAH) accumulation. Therefore, although overlap may exist, the cholic acid--uptake mechanism differs from the PAH-uptake mechanism in both the primate ciliary body and the primate iris.

Animals↗

PubMed1979

A highly specific 125I-radioimmunoassay for cholic acid conjugates.

Several modifications of the immunization procedure permitted development of a highly specific radioimmunoassay (RIA) for cholic acid conjugates. Antiserum was produced in guinea pigs using cholic acid-thyroglobulin complex as immunogen. 125-I-Cholyglycylhistamine was prepared as radioactive ligand according to a modification of the method of Spenney et al. (Spenney, J.G., Johnson, B.J., Hirschowitz, B.I., Mihas, A.A. and Gibson, R. (1977) Gastroenterology 72, 305--311). The association constant of the antisera to taurocholic acid was 1.8 x 10(7) l/mol, the working range of the assay between 9.5--890 pmol. Cross-reactivities of the antiserum to bile acids other than cholic acid species were less than 3%, which is lower than for any published bile acid RIA. Concentrations of cholic acid conjugates in sera obtained from 17 healthy fasting volunteers ranged from 0.4--1.9/mumul/l.

Animals↗

PubMed1979

Radioimmunoassay of conjugated cholic acid, chenodeoxycholic acid, and deoxycholic acid from human serum, with use of 125I-labeled ligands.

We describe a method for radioimmunoassay of conjugated cholic acid, chenodeoxycholic acid, and deoxycholic acid in serum. In the method, 125I-labeled bile acid conjugates are used as the tracers along with antibodies raised against individual bile acid-bovine serum albumin conjugates. Antibody-bound and free bile acids were separated by polyethylene glycol precipitation (final concentration, 125 g/L). Before radioimmunoassay, 0.1-mL serum samples were precipitated with nine volumes of ethanol, and portions from the supernate were used in the assays. The lowest measurable amounts of the bile acids, expressed as pmol/tube, were: cholic acid conjugates, 2; chenodeoxycholic acid conjugates, 0.5; and deoxycholic acid conjugates. 2. Analytical recovery of bile acids added to bile acid-free serum ranged from 85 to 110%; intra-assay and inter-assay CVs ranged from 3.2 to 5.3% and from 5.3 to 12.2%, respectively. Concentrations (mean +/- SD) of the bile acid conjugates in serum from apparently healthy women and men (in mumol/L) were: cholic acid conjugates, 0.43 +/- 0.17 (n = 126); chenodeoxycholic acid conjugates, 0.47 +/- 0.23 (n = 111); and deoxycholic acid conjugates, 0.33 +/- 0.11 (n = 96). The values for primary bile acids were greatly increased in patients with various hepatobiliary diseases.

Chenodeoxycholic Acid↗

PubMed1994

Effects of cholic acid and 'Protectaid' formulations on human sperm motility and ultrastructure.

Cholic acid (sodium cholate) and the other active ingredients of F-5 gel preparations in use for the impregnation of a new vaginal sponge (Protectaid) with contraceptive and anti-sexually transmitted disease properties, were assessed for their effects on human sperm motility and ultrastructure. Cholic acid (CA) produced an inhibition of motility which was both dose- and time-dependent. A complete suppression of motility was obtained at 30 s by a CA concentration of 1.25%. Nonoxynol-9 (NX9) compared with benzalkonium chloride (BZC) showed no significant difference at the concentration required (0.025%) to give a total inhibition of sperm motility after exposure for 30 s. The addition of F-5A gel containing 0.5% of each one of the spermicide ingredients (CA, NX9 and BZC) produced the total suppression of sperm motility within 30 s at a dilution of 1/50. Another preparation, F-5B gel, containing the spermicide ingredients at different concentrations (1.25% CA, 0.125% NX9 and 0.05% BZC) produced this same effect with a 1/10 dilution. Exposure of semen to a CA concentration of 1.25% or to 1/10 dilutions of F-5A gel for 30 s led to profound changes of sperm ultrastructure studied by scanning (SEM) and transmission (TEM) electron microscopy. SEM and TEM findings indicate that CA acts as a spermicide through its 'natural detergent' properties, damaging the outer plasma membrane of sperm cells. Protectaid formulations affect sperm motility and viability in a similar way.

Acrosome↗

PubMedDate not supplied

[Serum cholic acid levels in patients with acute leukemia].

In 34 patients (16 women and 18 men) with acute leukaemias (8 with acute lymphoblastic leukaemia and 26 with acute myeloblastic leukaemia), as yet untreated, the serum levels were determined of conjugated cholic acid, bilirubin, aspartate aminotransferase (AspAT), alanine aminotransferase (AlAT), alkaline phosphatase (AP), lactate dehydrogenase (LDH) and cholinesterase (Chol). Serum conjugated cholic acid level was determined by radioimmunoassay. The mean values of AP and Chol activity were within the range of normal values in this laboratory, the values of AspAT and AlAT were slightly above this range, and LDH value exceeded twice this normal range. The mean bilirubin concentration was within normal range. The greatest changes were noted in conjugated cholic acid values, the mean value exceeded five times the upper normal range (1.0 mumol/l). In 30 patients (88%) the conjugated cholic acid level in the serum was above 1.0 mumol/l, in the remaining 4 cases it was above the mean value for the control group. No correlation was found between conjugated cholic acid and any of the determined parameters. These results point out that the serum level of conjugated cholic acid may be a valuable parameter for assessment of hepatocellular function in acute leukaemias.

Adolescent↗

PubMed1993

Reduction of aberrant crypt foci induced in rat colon with azoxymethane or methylnitrosourea by feeding cholic acid.

Recent studies in our laboratory have demonstrated that feeding cholic acid (CHA) to rats treated with a single dose of azoxymethane (AOM) reduces the growth of putative preneoplastic lesions, aberrant crypt foci (ACF), in a dose-dependent manner. This finding was unexpected since CHA has been reported to promote colon cancer in rats receiving multiple treatments of the colon carcinogen, methylnitrosourea (MNU). The main objective of the present investigation was to evaluate the effect of the type of carcinogen and treatment protocol on the induction and growth of ACF in conjunction with CHA treatment. Male Sprague-Dawley rats received 0, 1 or 2 treatments with AOM or MNU and were fed either the AIN-76A or AIN-76A plus 0.2% CHA diet for 4 weeks. The total number and average size of ACF were significantly reduced in CHA-fed animals regardless of the type or number of treatments of carcinogen. The greatest reduction of ACF due to CHA-feeding was seen in the distal colon. The average crypt multiplicity (number of crypts in each ACF) was not altered by diet or carcinogen treatment. Colonic cell proliferation (crypt height and number of mitotic figures) was significantly increased in CHA-fed animals compared to control diet animals. Therefore, feeding CHA for 4 weeks reduced the number and size of ACF in rats induced by 1 or 2 injections of AOM or MNU, despite stimulation of colonic cell proliferation. These findings suggest further investigation is needed to understand the mechanism of promotion by cholic acid and the value of number and growth characteristics of ACF as a biological endpoint in the pathogenesis of colon cancer.

Analysis of Variance↗

PubMed1988

An endogenous colon mitosis inhibitor and dietary calcium inhibit the increased colonic cell proliferation induced by cholic acid.

We have previously reported that a single intraperitoneal injection of the tripeptide pGlu-His-GlyOH (colon mitosis inhibitor (CMI] is followed by a transient reduction of cell proliferation in the colonic epithelium in mice. The effect of the tripeptide on accelerated cell proliferation in the colonic epithelium was tested during the acute response of the epithelial cells to a diet supplemented with cholic acid. The kinetics of this response was first examined with different amounts of calcium in the feed. We found an increased labeling index (LI) and mitotic rate 2 days after changing the diet, and this response was stronger in animals with a low-calcium cholic acid diet than in animals with cholic acid diet with a standard amount of calcium or a high-calcium cholic acid diet. After 2 weeks of treatment cell proliferation remained significantly elevated only in the animals with low-calcium cholic acid diet. The effect of CMI was tested 7 days after the change to a low-calcium cholic acid diet. Under these conditions a single dose of CMI (10(-12) mol per animal) was still followed by a transient reduction in the proliferative indices in the colonic epithelium. However, the decreases in LI was observed earlier after CMI treatment (at 2 h) in the animals fed a low-calcium cholic acid than in animals with a standard diet.

Animals↗

PubMed1990

Cholic acid and chenodeoxycholic acid transport in the hepatic acinus in rats. Effect of necrosis of zone 3 induced by bromobenzene.

The transport of cholic acid (CA) and chenodeoxycholic acid (CDC) and their influence on bile formation was investigated in rats treated with bromobenzene (BZ), a toxicant which selectively destroys zone 3 of the hepatic acinus. The necrosis equals 27-31% of the acinus cells. The absence of zone 3 in rats reduced the secretory rate maximum of CA and CDC by 18% (NS) and 25% (p less than 0.05), respectively. The maximum bile flow was not different from control during CA infusion but was lower during CDC infusion in BZ-treated animals. Although the bile acid concentration was lower in BZ-treated rats, only values obtained during the basal period and the beginning of the infusion reached the level of statistically significant difference. The bile salt-independent flow (BSIF) was not affected by the absence of zone 3. Our data suggest that zones 1 and 2 of the hepatic acinus can compensate for the secretion of CA and elaboration of BSIF when zone 3 is destroyed. However, necrosis of zone 3 reduces CDC secretion. Thus, the capacity for bile acid transport of the hepatocytes of different zones in the hepatic acinus may differ according to the circulating bile acid.

Animals↗