Role of liver in regulating distribution and excretion of manganese

Abstract

Rectal obstruction abolished the total-body loss of Mn54 in both manganese-loaded and jaundiced rats. Bile duct obstruction only diminished the excretion of the radioisotope, proving that several gastrointestinal routes excrete manganese. Excretion was exceedingly fast if the isotope was injected intraportally, but then the effect of bile ligation became enhanced. Furthermore, biliary ligation induced a rise followed by a decline in the concentration of Mn54 in the liver, whereas that of the natural metal (Mn55) increased. Ancillary experimentation linked these phenomena to absorption and rapid reexcretion of the metal. This enterohepatic circulation participated in regulating the excretion of Mn. The customary acceleration of excretion following moderate loads with Mn was abolished by blocking the bile duct. Acceleration could be induced in bile-ligated animals provided they were overloaded with metal. The sum of the data indicated that bile formation constitutes the main regulatory route under ordinary conditions, but, under conditions of overloading, auxiliary gastrointestinal routes participate.