2-[[(3α,5β,7α,12α)-3,7,12-Trihydroxy-24-oxocholan-24-yl]amino]ethansulfonsure

Clusters of slender, four-sided prisms from alcohol + ether

Crystals

Very soluble in water and ethanol; slightly soluble in ether and ethyl acetate

Freely soluble in water; soluble in alcohol; almost insoluble in ether and ethyl acetate

Decomposes about 125 °C

125 °C

Specific optical rotation: +24 deg at 20 °C/D (concentration = 3 mg in 100 mL water) /Sodium taurocholate/

Specific optical rotation: +25.6 deg at 20 °C/D /Barium taurocholate/

Specific optical rotation: +38.8 deg at 18 °C/D (concn = 2 mg in 100 mL alcohol)

Warning

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P301+P317, P330, and P501 (click each P-code to see the statement)

The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

SRP: Criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Sitosterol & taurocholate given together to rats inhibited cholesterol 7alpha-hydroxylase activity.

Chickens receiving taurocholate iv did not show active tubular excretion; however, it inhibited tubular excretioN of phenolsulfonphthaleiN & of n-methylnicotinamide.

In the anesthetized rat, the low incidence of erosions with indomethacin was markedly increased by concurrent gastric perfusion with acid saline & taurocholate.

When a combination of aspirin & taurocholic acid was introduced to 8 subjects the mean electrical potential difference also fell significantly from 38.6 1.8 mv to 17.9 1.8 mv, but mean duration of this change (27 min) was significantly longer than found after individual admin.

For more Interactions (Complete) data for TAUROCHOLIC ACID (14 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.5(SRC), determined from a log Kow of 0.20(2) and a regression-derived equation(3), indicates that taurocholic acid is expected to have very high mobility in soil(SRC). The pKa of taurocholic acid is 1.4(4), indicating that this compound will exist almost entirely in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Volatilization of taurocholic acid from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.3X10-21 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Taurocholic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.5X10-20 mm Hg at 25 °C(SRC), determined from a fragment constant method(3). Taurocholic acid absorbs UV light >290 nm(6) and, therefore, may be susceptible to direct photolysis on soil surfaces exposed to sunlight(SRC). Although various strains of bacteria can utilize the taurocholic acid ion as sole sources of carbon and energy for growth(7), insufficient data are available to predict the importance of biodegradation in the environment(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.5(SRC), determined from a log Kow of 0.20(2) and a regression-derived equation(3), indicates that taurocholic acid is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 5.3X10-21 atm-cu m/mole(SRC), developed using a fragment constant estimation method(3). A pKa of 1.4(5) indicates taurocholic acid will exist almost entirely in the anion form at pH values of 5 to 9(SRC). According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is low. Taurocholic acid absorbs UV light >290 nm(7) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). Taurocholic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(4). Although various strains of bacteria can utilize the taurocholic acid ion as sole sources of carbon and energy for growth(8), insufficient data are available to predict the importance of biodegradation in the environment(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), taurocholic acid, which has an estimated vapor pressure of 3.5X10-20 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase taurocholic acid may be removed from the air by wet and dry deposition(SRC).

The Koc of taurocholic acid is estimated as 1.5(SRC), using a log Kow of 0.20(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that taurocholic acid is expected to have very high mobility in soil. The pKa of taurocholic acid is 1.4(4), indicating that this compound will exist almost entirely in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).

/HUMAN EXPOSURE STUDIES/ Seven patients were investigated after cholecystectomy and exploration of the common bile duct to determine bile composition and excretion rates. An initial depression of the major components of bile stabilized by the sixth postoperative day. Feeding of para-aminobenzoic acid and taurocholic acid to these patients demonstrated an increase in excretion of total bile acids, taurine and glycine conjugates, cholates and deoxycholates. Para-aminobenzoic acid in the doses used failed to block glycine conjugation. Preferential conjugation of bile acid with glycine is due to a deficient taurine pool and not a preferential metabolic pathway.

An estimated BCF of 3 was calculated in fish for taurocholic acid(SRC), using a log Kow of 0.20(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for taurocholic acid is estimated as 5.3X10-21 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that taurocholic acid is expected to be essentially nonvolatile from water surfaces(2). Taurocholic acid's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Taurocholic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.5X10-20 mm Hg at 25 °C(SRC), determined from a fragment constant method(1).

/LABORATORY ANIMALS: Acute Exposure/ Membrane-associated cytotoxicity induced by hydrophobic bile salts is a major contributing factor leading to liver diseases. Administration of ursodeoxycholate reduces serum liver enzymes in chronic liver diseases but the nature of this effect is still unclear. Using alcohol metabolising enzymes as cellular markers, the hepatotoxic properties of hydrophobic bile salts and the putative hepatoprotective effect of ursodeoxycholate was examined. Two animal models of biliary retention, bile duct obstruction and choledochocaval fistula was used to investigate the effect of taurocholate on the hepatic alcohol metabolizing enzymes: cytosolic alcohol dehydrogenase, microsomal ethanol oxidizing system, catalase and aldehyde dehydrogenase before and after the infusion of taurocholic acid or tauroursodeoxycholic acid for two days period. Bile duct obstruction was found to be similar to or slightly exceeds choledochocaval fistula in the degree of retention. Following the taurocholic acid infusion, the serum alcohol dehydrogenase activity as well as microsomal ethanol oxidizing system and aldehyde dehydrogenase were greatly increased but the level of cytosolic alcohol dehydrogenase and catalase activities was found to be lower in either or both models in comparison with the control animals. However, the tauroursodeoxycholic acid infusion did not induce any significant changes in the levels of all the alcohol metabolizing enzyme activities in either or both models. These findings suggest that hydrophobic taurocholic acid (7alpha) affects the plasmalemma to allow leakage of cytosolic alcohol dehydrogenase into the blood circulation, stimulates the biosynthesis of microsomal ethanol oxidizing system and aldehyde dehydrogenase, and suppresses the biosynthesis of alcohol dehydrogenase and catalase. But in contrast, the hydrophilic tauroursodeoxycholic acid (7beta) provided hepatoprotective effect.

/LABORATORY ANIMALS: Acute Exposure/ It is claimed that apoA-I expression is repressed in mice by cholic acid (CA) and its taurine conjugate, taurocholic acid (TCA) via farnesoid X receptor (FXR) activation. We measured apoA-I expression in mice, hamsters, and rats treated with highly potent and selective synthetic FXR agonists or with TCA. All of the synthetic agonists bound to FXR with high affinity in a scintillation proximity assay. However, TCA did not compete with the radio ligand up to the highest concentration used (100 uM). The C-site regulatory region of apoA-I, through which FXR has been reported to regulate its expression, is completely conserved across the species investigated. In both male and female human apoA-I-transgenic mice, we reproduced the previously reported strong inhibition of human apoA-I expression upon treatment with the typical supraphysiological dose of TCA used in such studies. However, in contrast to some previous reports, TCA did not repress murine apoA-I expression in the same mice. Also, more-potent and -selective FXR agonists did not affect human or murine apoA-I expression in this model. In LDL receptor-deficient mice and Golden Syrian hamsters, selective FXR agonists did not affect apoA-I expression, whereas in Wistar rats, some even increased apoA-I expression. In conclusion, selective FXR agonists do not repress apoA-I expression in rodents. Repression of human apoA-I expression by TCA in transgenic mice is probably mediated through FXR-independent mechanisms.

Taurocholic acid absorbs UV light >290 nm(1) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). Taurocholic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Although the amide moiety of taurocholic acid can undergo hydrolysis to cholic acid and taurine by acids and bases(3), amides do not hydrolyze under environmental conditions (pH 5-9)(4).

Occupational exposure to taurocholic may occur through dermal contact with this compound at workplaces where taurocholic acid is produced or used. The general population may be exposed to taurocholic acid via ingestion of foods containing taurocholic acid(1).

Taurocholic acid has known human metabolites that include 2-[[(4R)-4-[(3R,5R,7R,10S,12S,13R)-7,12-Dihydroxy-10,13-dimethyl-3-sulfooxy-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoyl]amino]ethanesulfonic acid.

Gastrointestinal agents that stimulate the flow of bile into the duodenum (cholagogues) or stimulate the production of bile by the liver (choleretic).

Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action that depends on possessing both hydrophilic and hydrophobic properties.

Transported by carrier-mediated processes bidirectionally across mammalian proximal tubule.

After secretion into the biliary tract, bile acids are largely (95%) reabsobed in the intestine (mainly in the terminal ileum), returned to the liver, and then again secreted in bile (enterohepatic circulation).

The disposition kinetics of [(3)H]taurocholate ([(3)H]TC) in perfused normal and cholestatic rat livers were studied using the multiple indicator dilution technique and several physiologically based pharmacokinetic models. The serum biochemistry levels, the outflow profiles and biliary recovery of [(3)H]TC were measured in three experimental groups: (i) control; (ii) 17 alpha-ethynylestradiol (EE)-treated (low dose); and (iii) EE-treated (high dose) rats. EE treatment caused cholestasis in a dose-dependent manner. A hepatobiliary TC transport model, which recognizes capillary mixing, active cellular uptake, and active efflux into bile and plasma described the disposition of [(3)H]TC in the normal and cholestatic livers better than the other pharmacokinetic models. An estimated five- and 18-fold decrease in biliary elimination rate constant, 1.7- and 2.7-fold increase in hepatocyte to plasma efflux rate constant, and 1.8- and 2.8-fold decrease in [(3)H]TC biliary recovery ratio was found in moderate and severe cholestasis, respectively, relative to normal. There were good correlations between the predicted and observed pharmacokinetic parameters of [(3)H]TC based on liver pathophysiology (e.g. serum bilirubin level and biliary excretion of [(3)H]TC). In conclusion, these results show that altered hepatic /taurocholate/ pharmacokinetics in cholestatic rat livers can be correlated with the relevant changes in liver pathophysiology in cholestasis.

It has been reported that the adjuvant-induced inflammation could affect drug metabolism in liver. /The authors/ further investigated the effect of inflammation on drug transport in liver using taurocholate as a model drug. The hepatic disposition kinetics of [(3)H]taurocholate in perfused normal and adjuvant-treated rat livers were investigated by the multiple indicator dilution technique and data were analyzed by a previously reported hepatobiliary taurocholate transport model. Real-time RT-PCR was also performed to determine the mRNA expression of liver bile salt transporters in normal and diseased livers. The uptake and biliary excretion of taurocholate were impaired in the adjuvant-treated rats as shown by decreased influx rate constant k(in) (0.65 +/- 0.09 vs. 2.12 +/- 0.30) and elimination rate constant k(be) (0.09 +/- 0.02 vs. 0.17 +/- 0.04) compared with control rat group, whereas the efflux rate constant k(out) was greatly increased (0.07 +/- 0.02 vs. 0.02 +/- 0.01). The changes of mRNA expression of liver bile salt transporters were found in adjuvant-treated rats. Hepatic taurocholate extraction ratio in adjuvant-treated rats (0.86 +/- 0.05, n = 6) was significantly reduced compared with 0.93 +/- 0.05 (n = 6) in normal rats. Hepatic extraction was well correlated with altered hepatic ATP content (r(2) = 0.90). In conclusion, systemic inflammation greatly affects hepatic ATP content/production and associated transporter activities and causes an impairment of transporter-mediated solute trafficking and pharmacokinetics.

For more Absorption, Distribution and Excretion (Complete) data for TAUROCHOLIC ACID (6 total), please visit the HSDB record page.

Sodium salt is a lipase accelerator; Choleretic

Biochemical research; emulsifying agent in foods (not over 0.1%)

Sodium salt is a lipase accelerator. Also used as a method for the quantification of conjugated bile acids in dried blood spots using electrospray ionization-mass spectrometry. Choleretic

Ingested as a constituent of ox bile extract used as a food additive

For more Uses (Complete) data for TAUROCHOLIC ACID (6 total), please visit the HSDB record page.

The product of conjugation of cholic acid with taurine.

Isolation from bile.

Ethanesulfonic acid, 2-[[(3.alpha.,5.beta.,7.alpha.,12.alpha.)-3,7,12-trihydroxy-24-oxocholan-24-yl]amino]-: INACTIVE

Cholic acid, chenodeoxycholic acid, and deoxycholic acid constitute 95% of bile acids... The bile acids exist largely as glycine /75%/ and taurine /24%/ conjugates, the salts of which are called bile salts.

/Taurocholic acid/ occurs as a sodium salt in the bile.