Taurocholic acid

515.7

515.70

201-336-2

5E090O0G3Z

25505

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

153

0.20 at 25 deg C, pH 1

Solid

1.265g/cm3

125 °C (decomp)

1.565

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

3.5X10-20 mm Hg at 25 deg C (est)

LD50 in newborn rats: 380 mg/kg (Klaassen)

D18 +38.8° (c = 2 in alcohol)

Henry's Law constant = 5.3X10-21 atm-cu m/mole at 25 °C (est)

pKa = 1.4|pKa = 2

211.2 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|205.82 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|221.99 Ų [M-H]- [CCS Type: DT, Method: stepped-field]|207.6 Ų [M-H]- [CCS Type: DT, Method: single field calibrated]|200.7 Ų [M+H-2H2O]+ [CCS Type: DT, Method: single field calibrated]|204.6 Ų [M+H-H2O]+ [CCS Type: DT, Method: single field calibrated]|211.1 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated]

Very hygroscopic /commercial preparation/; hydrolyzed to cholic acid and taurine by acids and alkalies|Converted to taurocholic acid by treatment with sulfuric acid /Barium taurocholate/|Sweet taste with bitter aftertaste /Sodium taurocholate/|Amorphous; yellow color /Commercial preparation/|For more Other Experimental Properties (Complete) data for TAUROCHOLIC ACID (8 total), please visit the HSDB record page.

Stable to air

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.

LD50 Mice ip 620 mg/kg|LD50 Rat ip 450 mg/kg

The sodium salt of taurocholic acid is the chief ingredient of the bile of carnivorous animals(1).

Taurocholic acid's production and use as an emulsifying agent in foods, as a choleretic and as a biochemical research agent(1,2) may result in its release to the environment through various waste streams(SRC).

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).

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).

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 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).

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).

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).

Cholagogues and Choleretics; Detergents|Dried bile from the Himalayan bear (Yutan) has been used for centuries in China to treat liver disease. /Bile/

Gastrointestinal agents that stimulate the flow of bile into the duodenum (cholagogues) or stimulate the production of bile by the liver (choleretic). (See all compounds classified as Cholagogues and Choleretics.)|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. (See all compounds classified as Detergents.)

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

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.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/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.

Cholyltaurine

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.

Lipids -> Sterol Lipids [ST] -> Steroid conjugates [ST05] -> Taurine conjugates [ST0504]