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Bile alcohols feces

Chromatographic analysis of the polar sterol fractions of the bile and feces, in conjunction with gas-liquid chromatography (GLC)-mass spectrometry indicated two major components, 5P-cholestane-3a,7a,12a,25-tetrol and 5P-cholestane-3a,7a,12a,23,25-pentol, and a minor component, 5P-cholestane-3a, 7a,12a,24,25-pentol(18-21). Only minute amounts of 5P-cholestane-3a, 7a,12a,23R-tetrol, 5P-cholestane-3a,7a,12a,24R-tetrol, 5P-cholestane-3a,7a, I2a,24S-tetrol and 5P-cholestane-3a,7a,12a,25S,26-pentol have been detected (20-24). The presence of 5P-cholestane-3a,7a,12a,25-tetrol was positively identified by comparison with the synthesized sample prepared in our laboratory (20-22,24-27) (Fig.l). The predominent bile alcohol of the pentol fraction was 5P-cholestane-3a,7a,12a,23,25-pentol, amounting to approximately 80% by weight, while 5P-cholestane-3a,7a,12a,24,25-pentol accounted for approximately 20% of this fraction. The less abundant pentol was shown to be identical with 5P-cholestane-3a,7a,12a,24a,25-pentol, which had been prepared from 5P-cholestane-3a,7a,12a,25-tetrol (20,21). [Pg.208]

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]

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]

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]

In 1974, Setoguchi et al. found that patients with cerebrotendinous xanthomatosis had an impaired sjTithesis of bile acids and excreted large amounts of C27 bile alcohols in bile and feces [76]. Since then, a number of investigations have revealed the occurrence of bile alcohols in mammals. It is now recognized that, when new analytical methods are applied, traces of bile alcohols can be detected even in biological fluids from healthy humans. Table 3 lists all the known bile alcohols identified in mammals. [Pg.289]

Hashish is metabolized in the liver and is eliminated in bile and feces. Only a trace amount of hashish is detectable in urine. Hashish may affect the metabolism of dmgs that require protein binding. These include ethyl alcohol, barbiturates, amphetamines, cocaine, opiates, and atropine. [Pg.98]

In a second study by Prout and Howard (1985b), the tissue distribution and excretion of [ " C]-alcohol-Iabeled tefluthrin was followed after the oral administration of 10 mg/kg to four male and four female rats in com oil. The animals were individually housed in metabolism cages for daily collections of urine and feces over a 7-days period. Rats were terminated at the end of 7 days and individual tissues harvested for the determination of radioactivity. A further set of two males and two females were administered an oral dose of 1.0 mg/kg [ " C] alcohol-labeled tefluthrin, after bile duct cannulation. Urine, bile, and feces were collected for a period of 48 h. Signs of acute toxicity were observed in the 10 mg/kg rats. Males excreted slightly less in urine (26% vs. 33%) and more in feces (68% vs. 63%) than females. In the bile duct study, males excreted 5-16% and females 8-10% of total radioactivity. [Pg.54]

There are medical tests to determine whether you have been exposed to chlordecone and/or its breakdown product, chlordecone alcohol. Levels of chlordecone and/or chlordecone alcohol can be measured in blood, saliva, feces, or bile. Chlordecone levels in blood are the best indicator of exposure to chlordecone. Since chlordecone remains in the blood for a long time, the test is useful for a long time after exposure has stopped. Chlordecone can be detected in saliva only within the first 24 hours after exposure therefore, this test has limited use. Blood levels of chlordecone are a good reflection of total body content of chlordecone. However, the test is an unsatisfactory indicator of the amount of chlordecone to which you have been exposed because you cannot be sure how much chlordecone left your body between the time you were exposed and the time the test is performed. These tests cannot predict how your health may be affected after exposure. The tests are not done in routine medical examinations, but doctors can collect body fluid samples and send them to a university medical center or a medical laboratory for analysis. Refer to Chapters 2 and 6 for more information. [Pg.17]

Chlordecone and chlordecone alcohol (chlordecol) are excreted in the bile and eliminated via the feces of humans occupationally exposed to chlordecone (Blanke et al. 1978 Boylan et al. 1979 ... [Pg.118]

Some toxic agents such as Pb, Hg, other heavy metals, and many organic substances are excreted in the bile as conjugates to the intestinal tract for elimination in the feces. Other common routes of elimination include the lungs for gaseous (e.g., NH3) and volatile toxicants (e.g., alcohol, sweat, tears, and saliva), as well as breast milk and eggs in females. [Pg.216]

The extraction of bile acids from solid material, such as feces or tissues, requires a different approach since bile acids are likely to be firmly bound to bacteria or proteins. A variety of solvents have been used, such as alcoholic alkali (G14), toluene-acetic acid (E4), methanol-acetone (B35), and methanol-chloroform (El), sometimes with refluxing or Soxhlet extraction (B17, El). The state of ionization of the carboxyl group of bile salts, and thus the solvent pH, would be expected to affect the efficiency of extraction with organic solvents, with better extraction at acid pH. However, in practice an... [Pg.194]


See other pages where Bile alcohols feces is mentioned: [Pg.120]    [Pg.207]    [Pg.216]    [Pg.258]    [Pg.1786]    [Pg.290]    [Pg.134]    [Pg.107]    [Pg.115]    [Pg.116]    [Pg.118]    [Pg.210]    [Pg.24]    [Pg.317]    [Pg.90]    [Pg.4520]    [Pg.76]   
See also in sourсe #XX -- [ Pg.289 , Pg.290 ]




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Feces

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