||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.
||Pub. in Reproductive Toxicology, v8 n1 p25-40 Feb 94. See also AD-A266 504. Prepared in cooperation with California Univ., Davis. and Procter and Gamble Co., Cincinnati, OH. Miami Valley Labs. Sponsored by National Institutes of Health, Bethesda, MD. and Department of Agriculture, Washington, DC.
|NTIS Title Notes
||Reprint: Altered Maternal Zinc Metabolism Following Exposure to Diverse Developmental Toxicants (Revised).
||57B; 57Y; 57S
||PC A03/MF A01