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Results for “CHOLIC ACID”

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PubMed2005

Selective acylation of cholic acid derivatives with multiple methacrylate groups.

Bile acids in the family of steroid compounds can be chemically modified for biochemical and other applications. Derivatives of cholic acid with multiple methacrylate groups can be prepared by the use of methacrylic acid, methacryloyl chloride and methacryloyl anhydride as the acylating agents. The hydroxyl groups of cholic acid methyl ester and cholic acid ethylene glycol ester have been selectively acylated by changing the acylating agents and the number of substitutions have been varied by changing the amount of the acylating agents used. In the acylation reactions with methacryloyl chloride, the reactivity of secondary hydroxyl groups on the steroid skeleton of cholic acid derivatives follows the order of C3>C12>C7.

Acylation↗

PubMed1976

Further studies on the possible compartmentation of the precursor pool of cholesterol for the biosynthesis of cholic acid in the rat.

In vivo and in vitro experiments with rats were carried out to investie precursor for the biosynthesis of cholic acid. When rats with a bile-fistula were given a mixture of [2-14C]mevalonate and [1,2-3H]cholesterol intravenously, the 14C:3H ratio in cholic acid in both whole homogenate and cytosol prepared from their lives was higher than that in free cholesterol in any subcellular fraction of the livers. When [2-14C] mevalonate was administered intravenously to bile-fistula rats, the specific radioactivity of free cholesterol in the hepatic microsomal fraction exceeded that in any other fraction, and the specific radioactivity of biliary cholic acid was remarkably high, exceeding that of microsomal free cholesterol. In similar experiments with [4-14C] cholesterol, the specific radioactivity of free cholesterol in the hepatic microsomal fraction exceeded that in any other subcellular fraction and the specific radioactivity of biliary cholic acid was lower than that of free cholesterol in any hepatic subcellular fraction. Tissue suspensions of rat livers in Krebs-Ringer bicarbonate (pH 7.4)-5.5 mM glucose were incubated with [2-14C]mevalonate in O2-CO2 (95:5, v/v) at 37 degrees. The specific radioactivity of free cholesterol in the microsomal fraction prepared from the incubated tissue exceeded the specific radioactivities of free cholesterol in the other subcellular fractions. The estimated specific radioactivity of taurocholate formed during the incubation was far higher than that of microsomal free cholesterol. These data indicate that hepatic microsomal free cholesterol which was newly synthesized in situ was preferentially incorporated into cholic acid.

Animals↗

PubMedDate not supplied

[Reactivity of the liver to administration of cholic acid to rats subjected to polychloropinene expsoure for a long time].

It was found that in healthy rats cholic acid caused a moderately increased intensity of bile secretion and raised the content of bile acids in it. In animals with toxic hepatitis produced by a long-term action of the chemical poison polychlorpinene in a dose of 1/10 DL50 and following introduction to such rats of cholic acid in a dose of 30 mg/100 g an intensified elinination of cholates and cholesterol excretion were evident. Combined action of polychlorpinene and cholic acid was conductive to a reduced conjugation of cholic acid with taurine and to a greater conjugation with glycine, this being attended by an increased content of free bile acids in the bile.

Animals↗

PubMed1983

Low serum cholic acid concentration of Duchenne muscular dystrophy.

Serum bile acids of 15 patients with Duchenne muscular dystrophy (DMD) were analyzed by gas-liquid chromatography. The serum cholic acid values were unusually low (0.16 +/- 0.13 microM), even less than 0.01 microgram/ml in 4, compared with controls (1.47 +/- 0.17 microM). HDL-cholesterol was within normal limits. The low concentration of serum cholic acid may be causative of abnormal calcium mobilization in DMD. The intracellular calcium mobilization seems to be affected by serum cholic acid as indicated by the enhanced rate of loss of intracellular calcium from the muscle exposed to cholic acid, which acts as a calcium-ionophore and reversibly forms soluble complexes with calcium ions.

Adolescent↗

PubMed1976

A 25-hydroxylation pathway of cholic acid biosynthesis in man and rat.

This paper describes a pathway of cholic acid synthesis, in man and in the rat, which involves 25-hydroxylated intermediates and is catalyzed by microsomal and soluble enzymes. The subcellular localization, stereospecificity, and other properties of the enzymes involved were studied with liver fractions of normolipidemic subjects, cerebrotendinous xanthomatosis patients, and rats. 5beta-Cholestane-3alpha,7alpha,12alpha,25-tetrol was converted to 5beta-cholestane-3alpha,7alpha,12alpha,24beta,25-pentol by the microsomal fraction in the presence of NADPH and O2. 5beta-Cholestane-3alpha,7alpha,12alpha,24alpha,25-pentol, 5beta-cholestane-3alpha,7alpha,12alpha,-23xi,25-pentol, and 5beta-cholestane-3alpha,7alpha,12alpha,25,26-pentol were also formed. In the presence of NAD, 5beta-cholestane-3alpha,7alpha,12alpha,24beta,25-pentol, but not the other 5beta-cholestanepentols formed, was converted to cholic acid by soluble enzymes in good yield. These experiments demonstrate the existence of a pathway for side-chain degradation in cholic acid synthesis which does not involve hydroxylation at C-26 or the participation of mitochondria.

Animals↗

PubMed1999

Oral administration of cholic acid promotes growth of liver tumors initiated by diethylnitrosamine in rats.

The effect of dietary administration of cholic acid on tumorigenesis in the liver was investigated in male Fischer-344 rats after carcinogenic initiation by diethylnitrosamine (DEN); progression of liver tumors was examined in the rats fed 0.4% cholic acid-containing diet (CA group) and the rats fed standard diet (C group) at 15, 20 and 25 weeks after administration of DEN. The total bile acids and cholic acid in serum of CA group were 150 nmol/ml and 117 nmol/ml, being 31-fold and 51-fold higher than those in C group (p<0.0001, each). Serum AST and ALT were significantly higher in CA group than in C group at 15 weeks (p<0.01). Serum ALP was significantly higher in CA group than C group at each time point (p<0.01, each). Liver tumors, whose histology was hepatocellular carcinoma, developed at 15 weeks in both CA and C groups. However, tumor volume and tumor weight were significantly increased in CA group, compared to those in C group at each time point (p<0.001, p<0. 001, p<0.01, p<0.001, p<0.01 and p<0.05). The percentage of apoptotic cells in CA group at each time point was significantly lower than C group (p<0.05, p<0.01 and p<0.05). The percentage of bcl-2 positive tumor cells in C group at 20 weeks was 1.88+/-2.59%. However, it dramatically increased to 34.00+/-13.67% in CA group (p<0.0001). It was also higher in CA group than in C group at 15 and 25 weeks (p<0.05 and p<0.01). In addition, the bax-positive cells were higher in CA group than in C group at 20 weeks (p<0.05). These data suggest that oral administration of cholic acid promotes liver tumorigenesis initiated by DEN through reducing apoptosis mediated by overexpression of bcl-2.

Administration, Oral↗

PubMedDate not supplied

Cholic acid amelioration of light and electron microscopic hepatic lesions in experimental protoporphyria.

We studied the effects of cholic acid treatment on hepatic histology and ultrastructure in mice with griseofulvin-induced protoporphyria. After 5 weeks of feeding griseofulvin alone, control mice developed darkly pigmented livers which by light microscopy showed birefringent, brown pigment deposits in bile ducts and ductules, sinusoidal Kupffer cell aggregates, and occasionally in hepatocytes and bile canaliculi. Electron microscopy demonstrated aggregated protoporphyrin crystals at these sites as well as membrane blebs and reduction of microvilli in bile canaliculi. In contrast, experimental mice that were concomitantly fed cholic acid and griseofulvin developed no detectable pigment on light microscopy, only rare protoporphyrin crystals on electron microscopy and minimal bile canalicular abnormalities. This study suggests that protoporphyrin transport into bile is enhanced by cholic acid treatment and results in a significant reduction in hepatic protoporphyrin deposition and associated abnormalities of liver morphology.

Animals↗

PubMed1980

Effects of feeding cholic acid and chenodeoxycholic acid on cholesterol absorption and hepatic secretion of biliary lipids in man.

Chenodeoxycholic acid (CDCA), in contrast to cholic acid (CA), reduces cholesterol saturation of bile. The mechanisms for these differences were the object of this study. Investigations were carried out in nine white men; three nonobese subjects and one obese subject were fed a weight-maintenance diet, and five obese patients had a reduced caloric intake for weight reduction. They were given a daily dose of 750-1000 mg CDCA or CA for one month after which they received the other bile acid for another month. The effects of both bile acids on bile acid pool size and hepatic secretion rates of biliary lipids were determined. Total bile acid pools were increased markedly by both CDCA and CA, but to about the same degree for each. Thus, the superior action of CDCA for lowering saturation of bile could not be explained by its effect on the pool sizes of bile acids. On the other hand, hepatic secretion of cholesterol, both during feeding and fasting, was found to be reduced to a greater extent by CDCA than by CA. A theoretical mechanism by which CDCA might lower hepatic outputs of cholesterol is the inhibition of cholesterol absorption. To examine this possibility, cholesterol absorption was estimated by use of an intestinal perfusion technique. No differences were obtained between the two treatment periods for either percentage or net absorption of cholesterol; thus it is unlikely that decreased absorption could account for the reduced cholesterol secretion. Another possibility is that CDCA might affect the interrelations of the three biliary lipids differently than CA. This was explored by measurements of hepatic secretion rates of these lipids. We observed a linear relationship between the secretion rates of bile acids and cholesterol, cholesterol and phospholipids, and bile acids during both treatment periods. However, cholesterol:phospholipid ratios were higher during CA therapy than with CDCA, and they increased still more during fasting in most CA-treated subjects, but not with CDCA. This indicated that there is a marked difference between the two bile acids in the degree of coupling of cholesterol and phospholipids in fasting. We suggest that the reduction in bile sa;uration on CDCA is most likely the result of changes in the interrelations of the different biliary lipids at the site of their secretion and/or inhibition of cholesterol output from the liver because of suppressed cholesterol synthesis in this organ.

Bile↗

PubMed1991

[Determination of cholic acid in man-made bezoar by derivative spectrometry].

Cholic acid in man-made bezoar can be determined by the suggested first order derivative spectrometric method. The peak amplitude within 310-290 nm is independent of the other components and only varies linearly with cholic acid concentration. The method is simple and accurate with good reproducibility.

Animals↗

PubMed1990

Crystal and molecular structures of the inclusion compounds of cholic acid with methanol, ethanol and 1-propanol.

The 1:1 inclusion compounds of cholic acid with methanol (C24H40O5.CH4O), ethanol (C24H40O5.C2H6O) and 1-propanol (C24H40O5.C3H8O) crystallize in the P2(1)2(1)2(1) space group with unit-cell dimensions at 293 K: a = 15.198 (6), b = 11.625 (7), c = 14.560 (9) A; a = 14.653 (7), b = 11.739 (4), c = 15.045 (2) A; and a = 15.026 (2), b = 11.864 (9), c = 14.951 (4) A; Z = 4. The structures were solved using direct methods. Full-matrix least-squares refinement reduced the conventional R factor to values of 0.109, 0.066 and 0.071, respectively. The alcohol molecules are contained in cavities created by the cholic acid molecules and are involved in the hydrogen-bonding scheme consisting of five unique hydrogen bonds. Statistical disorder is observed for the ethanol and 1-propanol molecules.

1-Propanol↗

PubMed1981

Hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and biliary lipid composition in man: relation to cholesterol gallstone disease and effects of cholic acid and chenodeoxycholic acid treatment.

The present work was undertaken in order to study whether or not there is a relation between hepatic HMG CoA reductase, hepatic cholesterol concentration, and biliary lipid composition. In 55 patients (10 with adenomyoma of the gallbladder wall, 45 with cholesterol gallstones) a liver biopsy together with gallbladder and hepatic bile were obtained at laparotomy under standardized conditions. Of the gallstone patients, twelve had been treated with cholic acid and ten with chenodeoxycholic acid in a dose of 15 mg.kg-1.d-1 for 6-8 weeks prior to operation. Hepatic bile was supersaturated with cholesterol both in cholesterol gallstone patients and in patients with gallbladder adenomyoma. Treatment with cholic acid reduced the cholesterol saturation of hepatic bile, although supersaturation persisted. During chenodeoxycholic acid treatment, hepatic bile became unsaturated in most of the patients. Hepatic cholesterol concentration was about 20% higher in patients with cholesterol gallstone disease than in gallstone-free controls. During treatment with cholic acid or chenodeoxycholic acid, hepatic cholesterol concentration was normalized. Microsomal HMG CoA reductase activity was similar in males and females with cholesterol gallstone disease and not different from that seen in the gallstone-free controls. Treatment with chenodeoxycholic acid resulted in a 40% reduction of HMG CoA reductase activity. Cholic acid had no effect. In gallstone-free controls and in bile acid-treated but not in untreated gallstone patients, saturation of hepatic bile correlated with HMG CoA reductase activity. It is concluded that treatment with chenodeoxycholic acid but not with cholic acid results in unsaturated hepatic bile. This unsaturation may in part be explained by a decreased hepatic HMG CoA reductase activity.

Adult↗

PubMed1986

Effect of cholic acid on tumor in the Egyptian toad.

Egyptian toads, Bufo regularis, were fed with cholic acid (sodium salt) 3 times/week for 12 weeks at different dose levels (2.5, 5, and 10 mg/toad). Results obtained showed only 1 case in both the 5 and 10 mg/toad doses that gave a tumor. Toads receiving N-methyl-N-nitrosourea (MNU) 1 mg/toad, 3 times/week for 12 weeks had 36% ileum tumors (18 toads out of 50, without mortality). On the other hand, a higher dose of MNU (5 mg/toad) caused 50% mortality in the experimental animals. Toads treated with MNU at a dose level of 1 mg/toad were subjected to CA at dose levels of 2.5, 5, 10 mg/toad. They showed a 48, 66 and 76% higher incidence of ileum tumors at the three different dose levels, respectively. It is concluded that cholic acid has a promoting effect on ileum tumor evoked by MNU in toads as in mammals.

Animals↗

PubMed1988

Induction of beta-glucuronidase activity during dimethylhydrazine carcinogenesis and additive effects of cholic acid and indole.

The kinetic change of beta-glucuronidase (beta-G) activity was measured in mouse large intestinal mucosa during dimethylhydrazine (DMH) carcinogenesis with addition of cholic acid and/or indole. The experiment lasted 21 weeks. The enzyme activity began to increase significantly at 5th week after treatment of DMH with cholic acid and/or indole, and at 7th week with DMH alone. Then, increased activity remained the rest of the time. Mouse intestinal cancer induced by DMH injection are also shown to have an increased beta-G activity. The induction of beta-G activity in the early stage of DMH colon carcinogenesis and additive effects of cholic acid and/or indole may imply one mechanism of action of DMH as a carcinogen and cholic acid as a promoter in large intestinal cancer.

Adenocarcinoma↗

PubMed1979

Evidence that cholic acid CoA ligase is located asymmetrically on the cytoplasmic surface of hepatic microsomal vesicles.

The cholic acid CoA ligase activity of rat liver was quantitatively inactivated by proteolysis with pronase, chymotrypsin, subtilisin, or proteinase K in intact microsomal vesicles. Under the conditions employed, less than 14% of the lumenal mannose-6-phosphate phosphatase activity was lost, and the mannose-6-phosphate phosphatase activity remained highly latent. After microsomal integrity was disrupted with sodium deoxycholate, protease treatment resulted in a loss of greater than 74% of the mannose-6-phosphate phosphatase activity. Cholic acid CoA ligase activity was unaffected by preincubation of microsomes with sodium taurocholate under conditions that led to the complete expression of latent mannose-6-phosphate phosphatase activity. The data suggest that cholic acid CoA ligase activity is located on the cytoplasmic surface of hepatic microsomal vesicles.

Animals↗

PubMed2000

Cholic acid is accumulated spontaneously, driven by membrane deltapH, in many lactobacilli.

Many lactobacilli from various origins were found to apparently lack cholic acid extrusion activity. Cholic acid was accumulated spontaneously, driven by the transmembrane proton gradient. Accumulation is a newly identified kind of interaction between intestinal microbes and unconjugated bile acids and is different from extrusion and modification, which have been described previously.

Biological Transport↗

PubMed2001

Circular dichroism spectra of the achiral guest N-aryl-N-nitrosamines included in the crystal host matrices of cholic acid.

The crystalline inclusion complexes of cholic acid with three symmetric N-aryl-N-nitrosamines were prepared, and their X-ray structures were solved. As a result of chiral conformations adopted by the enclathrated guest nitrosamines, the solid-state CD spectra were measured in KBr disks. The observed Cotton effect sign, corresponding to the n-pi* transition, was correlated with the helicity of the twisted nitrosamine chromophore conjugated with the N-aryl substituent. In addition, the absolute configuration of the enantiomorphous crystals of N-benzyl-N-nitroso-4-chloroaniline was established on the basis of the solid-state CD and X-ray crystallographic results.

Carcinogens↗

PubMed1978

Effect of cholestyramine on bile acid kinetics in patients with portal cirrhosis of the liver. Evidence of a selective defect in the formation of cholic acid.

The kinetics of cholic acid (C) and chenodeoxycholic acid (CD) were studied in six patients with portal liver cirrhosis. The studies were conducted both before and after 5-6 weeks of treatment with cholestyramine (12 g/day). In keeping with previous observations, the pool size and formation of C showed subnormal values during the pretreatment period, while the production of CD was within normal limits. The pool sizes of C and CD did not change upon treatment with cholestyramine, but the mean total bile acid formation increased by a factor of about 2.5. The ratio between the amounts of C and CD synthesized remained essentially unchanged. Considering the therapeutic response previously observed in normal subjects and in patients with hyper-beta-lipoproteinemia, the present results suggest a selective impairment of the biosynthesis of C in patients with portal liver cirrhosis. It is suggested that the primary defect may reside in the 12alpha-hydroxylase enzyme system.

Aged↗

PubMed2000

Drug release from thermo-responsive self-assembled polymeric micelles composed of cholic acid and poly(N-isopropylacrylamide).

Cholic acid, conjugated with amine-terminated poly(N-isopropylacrylamide) (abbreviated as CA/ATPNIPAAm), was synthesized by a N, N'-dicyclohexyl carbodiimide (DCC)-mediated coupling reaction. Self-assembled CA/ATPNIPAAm micelles were prepared by a diafiltration method in aqueous media. The CA/ATPNIPAAm micelles exhibited a lower critical solution temperature (LCST) at 31.5 degrees C. Micelle sizes measured by photon correlation spectroscopy (PCS) were approximately 31.6+/-5.8 nm. The CA/ATPNIPAAm micelles were spherical and their thermal size transition was observed by transmission electron microscope (TEM). A fluorescence probe technique was used for determining the micelle formation behavior of CA/ATPNIPAAm in aqueous solutions using pyrene as a hydrophobic probe. The critical micelle concentration (CMC) was evaluated as 8.9 x 10(-2) g/L. A drug release study was performed using indomethacin (IN) as a hydrophobic model drug. The release kinetics of IN from the CA/ATPNIPAAm micelles revealed a thermo-sensitivity by the unique character of poly(N-isopropylacrylamide) i.e. the release rate was higher at 25 degrees C than at 37 degrees C.

Acrylic Resins↗