Lithocholic acid - CAS 434-13-9
Catalog number:
Not Intended for Therapeutic Use. For research use only.
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Molecular Weight:
Lithocholic acid is a toxic secondary bile acid, causes intrahepatic cholestasis, has tumor-promoting activity, its toxic effect can be protected after it activates the vitamin D receptor, PXR and FXR.
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B0084-117962 50 g $189 In stock
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Brife Description:
toxic secondary bile acid
White Solid
Lithocholate; 3alpha-Hydroxy-5beta-cholanic acid; 3alpha-Hydroxy-5beta-cholan-24-oic acid
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1.Lithocholic acid attenuates cAMP-dependent Cl- secretion in human colonic epithelial T84 cells.
Ao M1, Domingue JC1, Khan N2, Javed F2, Osmani K1, Sarathy J1, Rao MC3. Am J Physiol Cell Physiol. 2016 Apr 13:ajpcell.00350.2015. doi: 10.1152/ajpcell.00350.2015. [Epub ahead of print]
Bile acids (BAs) play a complex role in colonic fluid secretion. We showed that dihydroxy BAs, but not the monohydroxy BA, lithocholic acid (LCA), stimulate Cl-secretion in human colonic T84 cells (AJP 305:C447-56, 2013). In this study, we explored the effect of LCA on the action of other secretagogues in T84 cells. While LCA (50µM, 15') drastically (>90%) inhibited forskolin-stimulated short-circuit current (Isc), it did not alter carbachol -stimulated Isc. LCA did not alter basal Isc, transepithelial resistance, cell viability or cytotoxicity. LCA's inhibitory effect was dose-dependent, acted faster from the apical membrane, rapid and not immediately reversible. LCA also prevented the Isc stimulated by the cAMP-dependent secretagogues, 8Br-cAMP, lubiprostone or chenodeoxycholic acid (CDCA). The LCA inhibitory effect was BA-specific, since CDCA, cholic acid or taurodeoxycholic acid did not alter forskolin or carbachol action. While LCA alone had no effect on [cAMP]i, it decreased forskolin-stimulated [cAMP]iby 90%.
2.Catalytic activity and thermal stability of horseradish peroxidase encapsulated in self-assembled organic nanotubes.
Lu Q1, Kim Y2, Bassim N3, Raman N1, Collins GE1. Analyst. 2016 Mar 21;141(7):2191-8. doi: 10.1039/c5an02655e.
Horseradish peroxidase (HRP) was encapsulated in self-assembled lithocholic acid (LCA) based organic nanotubes and its catalytic activity before and after thermal treatment was measured for comparison with free HRP. The apparent kcat (kcat/Km) for nanotube encapsulated HRP remained almost the same before and after thermal treatment, reporting an average value of 3.7 ± 0.4 μM(-1) s(-1). The apparent kcat value for free HRP decreased from 14.8 ± 1.3 μM(-1) s(-1) for samples stored at 4 °C to 2.4 ± 0.1 μM(-1) s(-1) after thermal treatment for 8 h at 55 °C. The Michaelis-Menten constants, Km, determined for encapsulated HRP and free HRP were relatively unperturbed by storage conditions at 4 °C or thermally treated at 55 °C for varying time periods from 2-8 h, with encapsulated HRP having a slightly higher Km than free HRP (13.4 ± 0.9 μM versus 11.7 ± 0.4 μM). The amount of HRP encapsulated in LCA nanotubes increased dramatically when the mixture of HRP and LCA nanotubes was brought to an elevated temperature.
3.Effect of Wheat Dietary Fiber Particle Size during Digestion In Vitro on Bile Acid, Faecal Bacteria and Short-Chain Fatty Acid Content.
Dziedzic K1, Szwengiel A2, Górecka D3, Gujska E4, Kaczkowska J3, Drożdżyńska A5, Walkowiak J6. Plant Foods Hum Nutr. 2016 Feb 29. [Epub ahead of print]
The influence of bile acid concentration on the growth of Bifidobacterium spp. and Lactobacillus spp. bacteria was demonstrated. Exposing these bacteria to the environment containing bile acid salts, and very poor in nutrients, leads to the disappearance of these microorganisms due to the toxic effect of bile acids. A multidimensional analysis of data in the form of principal component analysis indicated that lactic acid bacteria bind bile acids and show antagonistic effect on E. coli spp. bacteria. The growth in E. coli spp. population was accompanied by a decline in the population of Bifidobacterium spp. and Lactobacillus spp. with a simultaneous reduction in the concentration of bile acids. This is direct proof of acid binding ability of the tested lactic acid bacteria with respect to cholic acid, lithocholic acid and deoxycholic acid. This research demonstrated that the degree of fineness of wheat dietary fibre does not affect the sorption of bile acids and growth of some bacteria species; however, it has an impact on the profile of synthesized short-chained fatty acids.
4.Taurocholic acid metabolism by gut microbes and colon cancer.
Ridlon JM1,2,3, Wolf PG1,2,3,4, Gaskins HR1,2,3,4,5. Gut Microbes. 2016 Mar 22:1-15. [Epub ahead of print]
Colorectal cancer (CRC) is one of the most frequent causes of cancer death worldwide and is associated with adoption of a diet high in animal protein and saturated fat. Saturated fat induces increased bile secretion into the intestine. Increased bile secretion selects for populations of gut microbes capable of altering the bile acid pool, generating tumor-promoting secondary bile acids such as deoxycholic acid and lithocholic acid. Epidemiological evidence suggests CRC is associated with increased levels of DCA in serum, bile, and stool. Mechanisms by which secondary bile acids promote CRC are explored. Furthermore, in humans bile acid conjugation can vary by diet. Vegetarian diets favor glycine conjugation while diets high in animal protein favor taurine conjugation. Metabolism of taurine conjugated bile acids by gut microbes generates hydrogen sulfide, a genotoxic compound. Thus, taurocholic acid has the potential to stimulate intestinal bacteria capable of converting taurine and cholic acid to hydrogen sulfide and deoxycholic acid, a genotoxin and tumor-promoter, respectively.
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CAS 434-13-9 Lithocholic acid

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