Registration Dossier
Registration Dossier
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EC number: 292-588-2 | CAS number: 90640-67-8
Specific investigations: other studies
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:
- 1 998
- 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 substance name:
- Unknown substances
- Molecular formula:
- Not applicable
- IUPAC Name:
- Unknown substances
Constituent 1
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.
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