Oral mercuric chloride exposure in mice: effects of dose on intestinal absorption and relative organ distribution.

Human intoxications with inorganic mercury occur via the oral or pulmonar routes. However, earlier experimental studies of the acute toxicity of inorganic mercury primarily used parenteral administration of soluble inorganic mercury salts. The present study evaluated the effect of dose size on intestinal absorption and relative organ distribution of orally administered mercuric chloride. Experiments were performed with male mice of 2 strains (inbred CBA/Bom and outbred Bom: NMRI). At the highest dose of HgCl2, a delay in fecal elimination of non-absorbed mercury was observed indicating a decreased peristaltic rate. The fractional whole-body retention of mercury at 14 days after dosage was inversely related to the dose size, conceivably due either to saturation of the uptake mechanism or to damage to the kidneys resulting in loss of mercury with the urine at the highest dose levels. The relative organ distribution of mercury after oral exposure was quantitatively different from that reported in the literature after parenteral administration of inorganic mercury. Thus, the relative hepatic deposition was larger than after injection of mercury, presumably due to the first pass effect. A dose dependency in the relative organ distribution of retained mercury was observed, characterized by increasing relative deposition in liver, stomach, intestines, testes, spleen and carcass but decreasing relative renal deposition with increasing dose. The toxicokinetics of inorganic mercury was similar in the 2 mice strains. The present study demonstrates that the toxicokinetics of orally administered inorganic mercury is different from that of parenterally administered inorganic mercury as earlier reported in the literature.