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  • Title: Diversion or prevention of biliary outflow from the liver diminishes the renal uptake of injected inorganic mercury.
    Author: Zalups RK, Barfuss DW.
    Journal: Drug Metab Dispos; 1996 Apr; 24(4):480-6. PubMed ID: 8801064.
    Abstract:
    In the present study, we tested the hypothesis that diversion of biliary flow from the liver to the intestines (using biliary cannulation) or prevention of biliary outflow from the liver ( by biliary ligation) affects significantly the renal uptake and accumulation of mercury in rats given an intravenous nontoxic (0.5 mumol/kg) dose of mercuric chloride (containing 203 HgCl2). Diverting biliary flow away from the small intestine, by cannulation of the bile duct, caused a significant increase in the content of mercury in the blood and caused a significant decrease in the total renal uptake of mercury at 1 and 3 hr after the injection of mercuric chloride. By the end of 3 hr after the injection of mercury, the amount of mercury that was not taken up by the kidneys, as a result of diversion of biliary flow, was approximately 10% of the administered dose. The decreased renal uptake of mercury was caused by decreased uptake of mercury in the renal cortex and outer stripe of the outer medulla. Interestingly, very little mercury was excreted in the bile. Only approximately 0.19% of the administered dose of mercury was excreted in the bile in 3 hr. Renal accumulation of mercury, particularly in the cortex and outer stripe of the outer medulla, was also reduced significantly after biliary ligation, when evaluated 24 hr after the injection of inorganic mercury. There was an almost 3-fold increase in the content of mercury in the liver of the rats whose bile duct had been ligated. Fecal excretion of mercury was also diminished in these animals. It was interesting, however, that these rats did excrete some mercury in the feces. Dispositional data obtained from the segments of the gastrointestinal tract indicate that fecal excretion of mercury in the rats whose bile duct had been ligated was most likely caused by intestinal secretion of mercury. In conclusion, the present findings indicate that a hepato-biliary-enteric metabolic pathway plays a role in some aspect of the renal accumulation of administered inorganic mercury. This role does not, however, seem to involve, to any significant degree, the biliary and enteric processing of mercury secreted into the bile.
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