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American Journal of Clinical Nutrition, Vol 67, 1003S-1011S, Copyright © 1998 by The American Society for Clinical Nutrition, Inc
REVIEW ARTICLES |
CL Keen, JY Uriu-Hare, SN Hawk, MA Jankowski, GP Daston, CL Kwik-Uribe and RB Rucker
Department of Nutrition, University of California, Davis 95616, USA. clkeen@ucdavis.edu
Copper deficiency during embryonic and fetal development can result in numerous gross structural and biochemical abnormalities. Such a deficiency can arise through a variety of mechanisms, including low maternal dietary copper intake, disease-induced or drug-induced changes in maternal and conceptus copper metabolism, or both. These issues are discussed in this article along with the use of in vitro embryo culture models to study the mechanisms underlying copper deficiency-induced teratogenesis. Current data suggest that changes in free radical defense mechanisms, connective tissue metabolism, and energy production can all contribute to the dysmorphogenesis associated with developmental copper deficiency.
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