Amines, polyethylenepoly-, triethylenetetramine fraction

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:

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

Test material information

Constituent 1

Reference substance name:

Unknown substances

Molecular formula:

Not applicable

IUPAC Name:

Unknown substances

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.