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Urine bile alcohols

Bile alcohols are polyhydroxy C27 sterols that serve as intermediates in the biosjmthesis of cholic acid and chenodeoxycholic acid from cholesterol (1, 2). Recently several studies have shown that increased amounts of bile alcohols namely 27-nor-5p-cholestane-3a,7a,12a,24, 25-pentol and 5P-cholestane-3a, 7a,12a,25,26-pentol are excreted (as glucuronides in urine of patients with liver diseases such as primary biliary cirrhosis (3), liver cirrhosis (4, 5) and a-antitrypsin deficiency (6). Ichimiya et. al., described the occurrence of 5P-cholestane-3a,7a,12a,26,27-pentol (5P-cyprinol) and 5P-cholestane-3a,7a,... [Pg.207]

In summary, these studies demonstrated that in CTX the impaired synthesis of bile acids is due to a defect in the biosynthetic pathway involving the oxidation of the cholesterol side-chain. As a consequence of the inefficient side-chain oxidation, increased 23, 24 and 25-hydroxylation of bile acid precursors occurs with the consequent marked increase in bile alcohol glucuronides secretions in bile, urine, plasma and feces (free bile alcohols). These compounds were isolated, synthesized and fully characterized by various spectroscopic methods. In addition, their absolute stereochemistiy determined by Lanthanide-Induced Circular Dichroism (CD) and Sharpless Asymmetric Dihydroxylation studies. Further studies demonstrated that (CTX) patients transform cholesterol into bile acids predominantly via the 25-hydroxylation pathway. This pathway involves the 25-hydroxylation of 5P-cholestane-3a,7a, 12a-triol to give 5P-cholestane-5P-cholestane-3a,7a,12a,25- tetrol followed by stereospecific 24S-hydroxylation to yield 5P-cholestane-3a,7a,12a,24S,25-pentol which in turn was converted to cholic acid. [Pg.222]

Ichimiya, H., Yanagisawa, J. and Nakayama, F. (1984). Significance of bile alcohols in urine of a patient with cholestasis identification of Sp-cholestane-3a,7a,12a,26,27-pentol (5p-bufoI) and 5P-cholestane-3a,7a, 12a,26-tetrol (27-deoxy-5P-cyprinol). Chem. Pham. Bull. 32 2874-2877. [Pg.225]

Shimazu, K., Kuwabara, M., Yoshi, M., Kihira, K., Takeuchi, H., Nakano, I., Ozawa, S., Onuki, M., Hatta, Y., and Hoshita, T. (1986). Bile alcohol profiles in bile, urine, and feces of a patient with cerebrotendinous xanthomatosis. J. Biochem. (Tokyo) 99 477-483. [Pg.229]

To diagnose CTX, advantage has been taken of the elevated cholestanol levels in plasma. If the ratio of cholestanol to cholesterol is measured by gas-liquid chromatography, a value of over 1% is obtained in patients with CTX compared with less than 0.5% for normal subjects (S2). More recently, capillary gas-liquid chromatography has been used to detect bile alcohol conjugates in the urine of CTX patients and this technique has been useful to assess the efficacy of treatment with orally administered chenodeoxycholic acid (W12). [Pg.181]

The presence of bile alcohols in human urine was first demonstrated in 1981 by Karlaganis et al. [78]. Studying metabolic profiles of bile acids in urine, they found a number of bile alcohols in the steroid glucuronide fraction. The major compound was identified as 27-nor-5 6-cholestane-3a,7a,12a,24,25-pentol [78]. Excretion of this Cjf, bile alcohol as the major bile alcohol in urine from healthy and diseased humans was confirmed by Karlaganis et al. [79] and by Ludwig-Kohn et al. [94]. The latter authors also identified 5)8-cholestane-3a,7a,12a,25,26-pentol in human urine [94]. [Pg.290]

Y. Yang, W. J. Griffiths, H. Naza-, and J. SjOvall, Analysis of bile acids and bile alcohols in urine by capillary liquid chromatography-mass spectrometry using fast atom bombardment or electrospray ionization and collision induced dissociation, Biomed. Chromatogr. 11, 240-255 (1997). [Pg.451]

Allyl chloride is presumed to be metabolized to allyl alcohol, which could then be further metabolized via two pathways to form either acrolein or glycidol, from which a variety of metabolites could result. Metabolites identified in rat urine are 3-hydroxy-propylmercapturic acid and allyl mercapturic acid and its sulfoxide. Allyl glutathione and S-allyl-L-cysteine have been detected in the bile of dosed rats. In-vitro metabolism of allyl chloride results in haem destruction in microsomal cytochrome P450 (lARC, 1985). [Pg.1233]

Oral bioavailability of mibefradil is dose dependent and ranges from 37% to over 90% with doses of 10 mg or 160 mg, respectively. The plasma half-life is 17 to 25 hours after multiple doses, and it is more than 99% protein bound (15). The metabolism of mibefradil is mediated by two pathways esterase-catalyzed hydrolysis of the ester side chain to yield an alcohol metabolite and CYP3A4-catalyzed oxidation. After chronic dosing, the oxidative pathway becomes less important and the plasma level of the alcohol metabolite of mibefradil increases. In animal models, the pharmacological effect of the alcohol metabolite is about 10% compared to that of the parent compound. After metabolic inactivation, mibefradil is excreted into the bile (75%) and urine (25%), with less than 3% excreted unchanged in the urine. [Pg.714]

From 1966 to 1986 Horning was Director of the Institute of Lipid Research, Chairman of the Biochemistry Department (1962-1966), and Professor of Chemistry at Baylor College of Medicine (1961-1986). During this period he applied gas chromatography to steroids in human fluids, urine, bile and spinal liquids, and to amino add derivatives. His group isolated acids, alcohols, and waxes from human skin. Here they applied mass spectrometry and liquid or gas chromatography to the identification of numerous human substances. They extended these techniques to investigations of the metabolism of many different compounds in humans. [Pg.302]

Disposition in the Body. Readily absorbed after oral administration bioavailability about 65%. Haloperidol is localised in the tissues and rapidly taken up by the brain. It is slowly excreted in the urine, about 40% of a dose being eliminated in 5 days with only about 1% of the dose as unchanged drug about 15% of a dose is excreted in the bile. Metabolites which have been identified in urine are 4-fluorobenzoylpropionic acid and 4-fluorophenylaceturic acid (the glycine conjugate of 4-fluoro-phenylacetic acid), both of which are inactive. Haloperidol is also metabolised by reduction of the ketone group to a secondary alcohol. [Pg.648]

Lineomycin hydrochloride occurs as the monohydiate. a white, crystalline solid that is stable in the dry state. It is readily soluble in water and alcohol, and its aqueous solutions arc stable at room temperature. It is degraded slowly in acid solutions but is absorted well from the ga.strointesti-nal tract. Lineomycin diffuses well into peritoneal and pleural fluids and into bone. It is excreted in (he urine and the bile. It is available in capsule form for oral administration and in ampules and vials for parenteral administration. [Pg.354]

Vitamin A is readily absorbed from the intestine as retinyl esters. Peak serum levels are reached 4 h after ingestion of a therapeutic dose. The vitamin is distributed to the general circulation via the lymph and thoracic ducts. Ninety percent of vitamin A is stored in the liver, from which it is mobilized as the free alcohol, retinol. Ninety-five percent is carried bound to plasma proteins, the retinol-binding protein. Vitamin A undergoes hepatic metabolism as a first-order process. Vitamin A is excreted via the feces and urine. Beta carotene is converted to retinol in the wall of the small intestine. Retinol can be converted into retinoic acid and excreted into the bile and feces. The elimination half-life is 9 h. [Pg.2838]


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See also in sourсe #XX -- [ Pg.289 , Pg.290 ]




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Bile alcohols

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