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Lithocholic acid-d4 is intended for use as an internal standard for the quantification of lithocholic acid by GC- or LC-MS. 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.4,2,5

1.Little, J.M., Zimniak, P., Shattuck, K.E., et al.Metabolism of lithocholic acid in the rat: Formation of lithocholic acid 3-O-glucuronide in vivoJ. Lipid. Res.31(4)615-622(1990) 2.Makishima, M., Lu, T.T., Xie, W., et al.Vitamin D receptor as an intestinal bile acid sensorScience296(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 carcinogenCarcinogenesis21(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 toxicityProc. Natl. Acad. Sci. USA98(6)3369-3374(2000) 5.Tan, K.P., Yang, M., and Ito, S.Activation of nuclear factor (erythroid-2 like) factor 2 by toxic bile acids provokes adaptive defense responses to enhance cell survival at the emergence of oxidative stressMol. Pharmacol.72(5)1380-1390(2007)

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