Bile exposure

Saarela, M. Virkajarvi, L Alakomi, H.L. Mattila-Sandhohn, T. Vaari, A. Suomalainen, T. Mattb, J. Influence of fermentation time, cryoprotectant and neutralization of cell concentrate on freeze-drying survival, storage stability, and acid and bile exposure of Bifidobacterium animalis ssp. lactis cells produced without milk-based ingredients. J. Appl. Microbiol. 2005, 99 (6), 1330-1339. 

In addition, bile exposure induced the overexpression of ABC-type multidrug transporters and the activity of bUe efflux pumps for bile salts extrusion (Ctr and BetA in Bifidobacterium) (Sanchez et al. 2008a Ruiz et al. 2009 Hamon et al. 2011, 2012 Koskenniemi et al. 2011). 

Figure 10.3. Response mechanisms specifically triggered by bile exposure in lactobacilli and bifidobacteria.

The kidney is an important organ for the excretion of toxic materials and their metaboHtes, and measurement of these substances in urine may provide a convenient basis for monitoring the exposure of an individual to the parent compound in his or her immediate environment. The Hver has as one of its functions the metaboHsm of foreign compounds some pathways result in detoxification and others in metaboHc activation. Also, the Hver may serve as a route of elimination of toxic materials by excretion in bile. In addition to the Hver (bile) and kidney (urine) as routes of excretion, the lung may act as a route of elimination for volatile compounds. The excretion of materials in sweat, hair, and nails is usually insignificant. 

The sheer complexity of environmental mixtnres of EDCs, possible interactive effects, and capacity of some EDCs to bioaccumulate (e.g., in fish, steroidal estrogens and alkylphenolic chemicals have been shown to be concentrated up to 40,000-fold in the bile [Larsson et al. 1999 Gibson et al. 2005]) raises questions about the adequacy of the risk assessment process and safety margins established for EDCs. There is little question that considerable further work is needed to generate a realistic pictnre of the mixture effects and exposure threats of EDCs to wildlife populations than has been derived from studies on individual EDCs. Further discussion of the toxicity of mixtures will be found in Chapter 2, Section 2.6. 

Following inhalation exposure to trichloroethylene in humans, the unmetabolized parent compound is exhaled, whereas its metabolites are primarily eliminated in the urine. Excretion of trichloroethylene in the bile apparently represents a minor pathway of elimination. Balance studies in humans have shown that following single or sequential daily exposures of 50-380 ppm trichloroethylene, 11% and 2% of the dose was eliminated unchanged and as trichloroethanol, respectively, in the lungs 58% was eliminated as urinary metabolites and approximately 30% was unaccounted for (Monster et al. 1976, 1979). Exhaled air contained notable concentrations of trichloroethylene 18 hours after exposure ended because of the relatively long half-life for elimination of trichloroethylene from the adipose tissue (i.e., 3.5-5 hours) compared to other tissues (Fernandez et al. 1977 Monster et al. 1979). 

Wang G, Stacey NH. 1990. Elevation of individual serum bile acids on exposure to trichloroethylene or a-naphthylisothiocyanate. Toxicol Appl Pharmacol 105 209-215. 

A study with a dog exposed to an occluded dermal dose of TOCP labeled with radioactive phosphorus provides limited evidence that organophosphate esters in hydraulic fluids may be widely distributed after dermal absorption (Hodge and Sterner 1943). Similar widespread distribution of radioactivity among tissues was observed in male cats after dermal exposure to [uniformly labeled 14C-phenyl]TOCP (Nomeir and Abou-Donia 1986). Tissues and fluids with the highest concentrations of radioactivity in these studies included the bile, gall bladder, urinary bladder, liver, kidney, and fat, thus suggesting that TOCP and metabolites are somewhat preferentially distributed to these tissues. 

Long exposure of workers to DBT moieties caused bile-duct damage and exposure to TPhT compounds caused liver damage34. This is probably due to high biliary excretion rate of butyltin compounds. 

Stehly, G.R. and W.L. Hayton. 1988. Detection of pentachlorophenol and its glucuronide and sulfate conjugates in fish bile and exposure water. Jour. Environ. Sci. Health B23 355-366. 

Orally ingested hexachloroethane is exhaled and excreted in mine and fecal matter. The portion of the hexachloroethane found in fecal matter is the result of excretion in bile. The results of studies that measured the amount of residual hexachloroethane in excreta can be misleading, since much of the absorbed hexachloroethane is metabolized to other compounds. Measurement of 14C label after exposure to labeled compound presents a more complete picture of ultimate hexachloroethane fate and excretion than measurement of hexachloroethane. 

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