| First Author | Nielsen JB | Year | 1998 |
| Journal | Analyst | Volume | 123 |
| Issue | 1 | Pages | 87-90 |
| PubMed ID | 9581026 | Mgi Jnum | J:45821 |
| Mgi Id | MGI:1196160 | Doi | 10.1039/a705215d |
| Citation | Nielsen JB, et al. (1998) Strain dependence of steady-state retention and elimination of mercury in mice after prolonged exposure to mercury(II) chloride. Analyst 123(1):87-90 |
| abstractText | Previous studies have demonstrated that the toxicokinetics of a single oral dose of inorganic mercury in mice depends on the specific strain. The strain dependent kinetics were attributed primarily to differences in intestinal Hg2+ absorption. Elimination kinetics have been difficult to evaluate, however, as the majority of a single oral dose will pass through the gastrointestinal tract unabsorbed. Therefore, in contrast to previous studies, in this study exposure to inorganic mercury in drinking water for a prolonged time period was used in order to reach a steady state for whole-body retention of mercury. The exposure level (5 mg l-1) was sufficiently low to exclude gastrointestinal toxicity. The steady-state retention of mercury was established in four inbred mouse strains (B10.S, DBA, A.SW and SJL). The DBA strain reached the highest whole-body steady state level of mercury (19 micrograms Hg) whereas B10.S mice, when considering the drinking water consumption, had the lowest steady-state retention of mercury (15 micrograms Hg). Analysis of the whole-body elimination of mercury after 12 weeks of drinking water exposure indicated that variations in the elimination kinetics could explain a large fraction of the observed strain differences in the steady-state retention of mercury. Thus, the approximate half-time for elimination of aged mercury depots was longest in DBA mice (83 d) and shortest in B10.S mice (44 d). Further, the observed organ depositions indicated that differences in the transport of mercury from the liver to kidney might also explain some of the differences in the elimination kinetics. |
