Steroids biliary

Retention of radiocopper injected into humans is high only 10% is excreted within 72 h in urine and feces, and 50% in four weeks (Aaseth and Norseth 1986). Most (72%) of the unabsorbed copper is excreted in the feces primarily by way of the biliary duct, the salivary glands, or the intestinal mucosa a minor portion is excreted by way of sweat and menses (Schroeder et al. 1966 USEPA 1980 ATSDR 1990). In mammals, copper is excreted mainly via the bile in association with glutathione or unidentified high-molecular-weight molecules. However, the transport mechanisms of copper from liver cells into bile are essentially unknown (Aaseth and Norseth 1986). In rats, biliary excretion of copper is increased by increased flow of bile, increased body temperature, or administration of adrenal steroids (Sugawara et al. 1994). 

When radioactively labeled steroids are injected intravenously in man, most of the radioisotope is recovered in the urine within 72 hours. Neither biliary nor fecal excretion is any of quantitative importance in man [63]. 

The intermediate-acting steroid muscle relaxants (eg, vecuronium and rocuronium) tend to be more dependent on biliary excretion or hepatic metabolism for their elimination. These muscle relaxants are more commonly used clinically than the long-acting steroid-based drugs (eg, pancuronium, pipecuronium). 

Kern F Jr, Everson GT, DeMark B, McKinley C, Showalter R, Braverman DZ, Szczepanik-Van Leeuwen P, Klein PD. Biliary lipids, bile acids, and gallbladder function in the human female effects of contraceptive steroids. J Lab Clin Med 1982 99(6) 798-805. 

Tanaka, K., Aso, B., and Sugano, M. 1984. Biliary steroid excretion in rats fed soybean protein and casein or their amino acid mixtures. J. Nutr. 114, 26-32. 

Another sinusoidal transporter catalyzes Na+-independent uptake of organic anions and is instrumental for biliary clearance of glucuronidated and sulfated steroids, the diagnostic chemical bromosulfophthalein (BSP) and possibly bilirubin. Canalicular transport of glucuronidate and GSH conjugates is coupled to ATP... 

Secondary hyperlipidaemias results from liver and biliary disease, obesity, hypothyroidism, diabetes, diet, alcohol excess, renal disease (nephrotic syndrome) and drugs (including etretinate, HIV protease ir hibitors, thiazide diuretics, oral contraceptive steroids, glucorticosteroids, (3-adrenoceptor antagonists, ciclosporin). 

In addition, biliary obstructive jaundice can also be caused by drug-induced toxicity, e.g. with Ciy-substi-tuted steroids, erythromycin estolate, chlorpromazine, chlorpropamide, ajmaline, halothane, methylthiouracil. 

Fusidic acid is the best-known representative of a group of antibiotics with steroid structures, which are eliminated primarily by biliary excretion as microbiologically inactive metabolites. The antibacterial action of fusidic acid is bacteriostatic, although it can be bactericidal at... 

Yet another classification system refers to the nature of the host s response to the causative agent. Some agents, referred to as intrinsic hepatotoxicants, will cause hepatotoxicity in most individuals of most species. In the case of idiosyncratic hepatotoxicants, where a chemical s toxic effects are a function of unusual susceptibility of the exposed individual, it may not be clear whether the lesion is a manifestation of the hepatotoxic properties of the substance in question or a manifestation of the individual s untoward response to the agent. This response may mean hypersensitivity (allergic) reactions or exaggerated responses to minor alterations in liver function. For example, anabolic or contraceptive steroids cause diminished biliary excretion (cholestasis) in most... 

Selye, H. (1972) Prevention by catatoxic steroids of lithocholic acid-induced biliary concrements in the rat. Proc. Soc. Exp. Biol. Med. 141, 555-558. 

In 1971, Makino et al. found that considerable amounts of 3jS-hydroxychol-5-en-24-oic acid were excreted in urine of children with extrahepatic biliary atresia [111]. Since then, the unsaturated C24 bile acid has been identified in human meconium [112,113], amniotic fluid [114,115], gallbladder bile from premature and term infants [116], urine from children and adults, both healthy and with liver disease [82,117], and bile and feces from newborn and fetal guinea pigs [118]. The natural occurrence of 3j8-hydroxychol-5-en-24-oic acid suggests that the side chain of cholesterol is degraded before modification of the steroid ring system (Chapter 9). 

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