Disposition of inorganic mercury following biliary obstruction and chemically induced glutathione depletion: dispositional changes one hour after the intravenous administration of mercuric chloride.

Influences of biliary obstruction and systemic depletion of glutathione (GSH) on the disposition of a low nontoxic iv dose of inorganic mercury were evaluated in rats in the present study. Specifically, the disposition of mercury in the kidneys, liver, small and large intestines, and blood was assessed 1 h after the injection of 0.5 micromol/kg mercuric chloride in control rats and rats pretreated with acivicin, buthionine sulfoximine (BSO), or diethylmaleate (DEM) that did or did not undergo acute biliary ligation prior to the injection of mercury. Among the groups that did not undergo biliary ligation, the pretreatments used to alter GSH status systemically had varying effects on the disposition of inorganic mercury in the kidneys, liver, intestines, and blood. Biliary ligation caused the net renal accumulation of mercury to decrease under all pretreatment conditions. By contrast, biliary ligation caused significant increases in the hepatic burden of mercury in all pretreatment groups except the acivicin-pretreated group. Blood levels of mercury also increased as a result of biliary ligation, regardless of the type of pretreatment used. Evidence for a secretory-like movement of mercury into the lumen of the intestines is also provided in the animals that underwent biliary ligation. The present findings indicate that biliary ligation combined with methods used to alter GSH status systemically have additive effects with respect to causing reductions in the net renal accumulation of mercury. In addition, the findings indicate that at least some fraction of the renal accumulation of inorganic mercury is linked mechanistically to the hepatobiliary system.