Registration Dossier

Administrative data

Endpoint:
specific investigations: other studies
Type of information:
other: review article
Adequacy of study:
supporting study
Reliability:
other: review article on copper deficiency and prenatal development

Data source

Reference
Reference Type:
publication
Title:
Effect of copper deficiency on prenatal development and pregnancy outcome
Author:
Keen, C.L., Uriu-Hare, J.Y., Hawk, S.N., Jankowski, M.A., Daston, G.P., Kwik-Uribe, C.L.., Rucker, R.B.
Year:
1998
Bibliographic source:
Am J Clin Nutr 1998;67(suppl):1003S–11S

Materials and methods

Principles of method if other than guideline:
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.
Endpoint addressed:
developmental toxicity / teratogenicity

Test material

Reference
Name:
Unnamed
Type:
Constituent

Results and discussion

Details on results:
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.

Applicant's summary and conclusion

Executive summary:

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.