||Altered Maternal Zinc Metabolism Following Exposure to Diverse Developmental Toxicants (Revised).
Taubeneck, M. W.;
Daston, G. P.;
Rogers, J. M.;
Keen, C. L.;
||Health Effects Research Lab., Research Triangle Park, NC. ;California Univ., Davis. ;Procter and Gamble Co., Cincinnati, OH. Miami Valley Labs.;National Institutes of Health, Bethesda, MD.;Department of Agriculture, Washington, DC.
Acute phase response
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
The hypothesis that hepatic metallothionein (MT) induction in the pregnant animal results in a zinc (Zn) deficiency in the embryo was tested by treating pregnant rats with alpha-hederin, reported to induce MT in rat liver. Morphological development was assessed in term fetuses. A single dose of alpha-hederin, of 3-300 micromodes/kg, caused a dosage-related increase in maternal hepatic MT. These data support the hypothesis that systematic changes in Zn status, brought about by induction of hepatic MT, maybe a mechanism for maternally-mediated abnormal development.