Pricing updated 2019-07-17. Prices are subject to change without notice.
Lithocholic acid is a secondary bile acid that has been shown to cause cholestasis in animal models and has also been implicated in carcinogenesis.1,2 It is produced from chenodeoxycholic acid by bacterial action in the colon and can be conjugated with glycine or taurine. Whereas in normal colonic epithelium lithocholic acid promotes apoptosis, it has been shown to suppress apoptosis in pre-malignant colonic epithelium in the presence of a carcinogen.3 Lithocholic acid can activate the pregnane X receptor and the vitamin D receptor, which may serve as a biological sensor to regulate lithocholic acid-induced toxicity.2,4,5
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Little, J.M., Zimniak, P., Shattuck, K.E., et al. Metabolism of lithocholic acid in the rat: Formation of lithocholic acid 3-
2. Makishima, M., Lu, T.T., Xie, W., et al. Vitamin D receptor as an intestinal bile acid sensor Science 296(5571), 1313-1316 (2002).
3. Kozoni, V., Tsioulias, G., Shiff, S., et al. The effect of lithocholic acid on proliferation and apoptosis during the early stages of colon carcinogenesis: Differential effect on apoptosis in the presence of a colon carcinogen Carcinogenesis 21(5), 999-1005 (2000).
4. Staudinger, J.L., Goodwin, B., Jones, S.A., et al. The nuclear receptor PXR is a lithocholic acid sensor that protects against liver toxicity Proc. Natl. Acad. Sci. USA 98(6), 3369-3374 (2000).
Tan, K.P., Yang, M., and Ito, S. Activation of nuclear factor (erythroid-