Abstract

Copper deficiency during pregnancy results in embryonic and fetal abnormalities as well as persistant effects on postnatal development. The long term objective of these studies is to understand the mechanisms of copper deficiency-induced abnormalities on embryonic development. The investigators will focus on oxidative mechanisms at a morphologic and mechanistic level the abnormalities in cardiovascular integrity observed in copper deficient embryos. In vitro culture methods will be used to elucidate the mechanisms by which copper-induced alterations in extracellular matrix modulate vascular growth and differentiation during blood vessel assembly. Furthermore, the investigators will study the role of select proteins in intracellular copper transport and metabolism in embryonic development using antisense technology. This information should provide new insights into the mechanisms underlying copper deficient pathologies and may contribute to our understanding of this process during human development.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
2R01HD026777-08
Application #
6197461
Study Section
Nutrition Study Section (NTN)
Program Officer
Grave, Gilman D
Project Start
1990-06-01
Project End
2005-06-30
Budget Start
2000-08-18
Budget End
2001-06-30
Support Year
8
Fiscal Year
2000
Total Cost
$243,090
Indirect Cost

  Institution

Name
University of California Davis
Department
Nutrition
Type
Schools of Earth Sciences/Natur
DUNS #
094878337
City
Davis
State
CA
Country
United States
Zip Code
95618

  Publications

Uriu-Adams, Janet Y; Scherr, Rachel E; Lanoue, Louise et al. (2010) Influence of copper on early development: prenatal and postnatal considerations. Biofactors 36:136-52
Keen, Carl L; Uriu-Adams, Janet Y; Skalny, Anatoly et al. (2010) The plausibility of maternal nutritional status being a contributing factor to the risk for fetal alcohol spectrum disorders: the potential influence of zinc status as an example. Biofactors 36:125-35
Yang, Soo Jin; Keen, Carl L; Lanoue, Louise et al. (2007) Low nitric oxide: a key factor underlying copper-deficiency teratogenicity. Free Radic Biol Med 43:1639-48
Beckers-Trapp, Molly E; Lanoue, Louise; Keen, Carl L et al. (2006) Abnormal development and increased 3-nitrotyrosine in copper-deficient mouse embryos. Free Radic Biol Med 40:35-44
Yang, Soo Jin; Uriu-Adams, Janet Y; Keen, Carl L et al. (2006) Effects of copper deficiency on mouse yolk sac vasculature and expression of angiogenic mediators. Birth Defects Res B Dev Reprod Toxicol 77:445-54
Uriu-Adams, Janet Y; Rucker, Robert B; Commisso, Joel F et al. (2005) Diabetes and dietary copper alter 67Cu metabolism and oxidant defense in the rat. J Nutr Biochem 16:312-20
Uriu-Adams, Janet Y; Keen, Carl L (2005) Copper, oxidative stress, and human health. Mol Aspects Med 26:268-98
Cui, Changtai T; Uriu-Adams, Janet Y; Tchaparian, Eskouhie H et al. (2004) Metavanadate causes cellular accumulation of copper and decreased lysyl oxidase activity. Toxicol Appl Pharmacol 199:35-43
Keen, Carl L; Clegg, Michael S; Hanna, Lynn A et al. (2003) The plausibility of micronutrient deficiencies being a significant contributing factor to the occurrence of pregnancy complications. J Nutr 133:1597S-1605S
Keen, Carl L; Hanna, Lynn A; Lanoue, Louise et al. (2003) Developmental consequences of trace mineral deficiencies in rodents: acute and long-term effects. J Nutr 133:1477S-80S

Showing the most recent 10 out of 35 publications