Abstract
Based on our findings of low SOD activity and high oxidative damage, we have suggested that reductions in oxidant defense represent one mechanism contributing to Cu deficiency-induced teratogenesis. In the current work, we tested the hypothesis that an additional mechanism could be impaired enorgy production as a consequence of Cu deficiency associated reductions in cytochrome c oxidase activity. Embryos were removed at gestation day 10 front dams fed either a control (+Cu) or Cu deficient (-Cu) diet (8.0 μg/g and <0.5 μg/g diet, respectively). The +Cu embryos were explanted into -+Cu sera. (19.2 μM) while -Cu embryos wore cultured in -Cu sera (1.2 μM) for 48 h. Kmbryos removed from -Cu dams and cultured in -Cu sera, had significantly lower cytochrome c oxidase activity (50% reduction) than +Cu embryos cultured in +Cu sera. To determine if the lower cytochrome c oxidase activity was functionally significant, ATP concentrations were determined in single embryos using a chemiluminescence assay. AT P concentrations were significantly lower in embryos from -Cu dams that were cultured in -Cu serum than those removed from +Cu dams that were cultured in +Cu serum. These data support the concept that the teratogenicity of Cu deficiency occurs through a number of mechanisms including impairments in energy production and oxidant detente. The role of Cu deficiency-induced alterations in other processes such as angiogenesis and extracellular matrix maturation needs to be investigated.
| Original language | English (US) |
|---|---|
| Journal | FASEB Journal |
| Volume | 11 |
| Issue number | 3 |
| State | Published - 1997 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Biochemistry
- Cell Biology
Cite this
Altered energy metabolism is an additional factor contributing to copper (Cu) deficiency-induced teratogenesis. / Hawk, S. N.; Kwik-Uribe, C. L.; Uriu-Hare, J. Y.; Daston, G. P.; Rucker, R. B.; Keen, Carl L.
In: FASEB Journal, Vol. 11, No. 3, 1997.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Altered energy metabolism is an additional factor contributing to copper (Cu) deficiency-induced teratogenesis
AU - Hawk, S. N.
AU - Kwik-Uribe, C. L.
AU - Uriu-Hare, J. Y.
AU - Daston, G. P.
AU - Rucker, R. B.
AU - Keen, Carl L
PY - 1997
Y1 - 1997
N2 - Based on our findings of low SOD activity and high oxidative damage, we have suggested that reductions in oxidant defense represent one mechanism contributing to Cu deficiency-induced teratogenesis. In the current work, we tested the hypothesis that an additional mechanism could be impaired enorgy production as a consequence of Cu deficiency associated reductions in cytochrome c oxidase activity. Embryos were removed at gestation day 10 front dams fed either a control (+Cu) or Cu deficient (-Cu) diet (8.0 μg/g and <0.5 μg/g diet, respectively). The +Cu embryos were explanted into -+Cu sera. (19.2 μM) while -Cu embryos wore cultured in -Cu sera (1.2 μM) for 48 h. Kmbryos removed from -Cu dams and cultured in -Cu sera, had significantly lower cytochrome c oxidase activity (50% reduction) than +Cu embryos cultured in +Cu sera. To determine if the lower cytochrome c oxidase activity was functionally significant, ATP concentrations were determined in single embryos using a chemiluminescence assay. AT P concentrations were significantly lower in embryos from -Cu dams that were cultured in -Cu serum than those removed from +Cu dams that were cultured in +Cu serum. These data support the concept that the teratogenicity of Cu deficiency occurs through a number of mechanisms including impairments in energy production and oxidant detente. The role of Cu deficiency-induced alterations in other processes such as angiogenesis and extracellular matrix maturation needs to be investigated.
AB - Based on our findings of low SOD activity and high oxidative damage, we have suggested that reductions in oxidant defense represent one mechanism contributing to Cu deficiency-induced teratogenesis. In the current work, we tested the hypothesis that an additional mechanism could be impaired enorgy production as a consequence of Cu deficiency associated reductions in cytochrome c oxidase activity. Embryos were removed at gestation day 10 front dams fed either a control (+Cu) or Cu deficient (-Cu) diet (8.0 μg/g and <0.5 μg/g diet, respectively). The +Cu embryos were explanted into -+Cu sera. (19.2 μM) while -Cu embryos wore cultured in -Cu sera (1.2 μM) for 48 h. Kmbryos removed from -Cu dams and cultured in -Cu sera, had significantly lower cytochrome c oxidase activity (50% reduction) than +Cu embryos cultured in +Cu sera. To determine if the lower cytochrome c oxidase activity was functionally significant, ATP concentrations were determined in single embryos using a chemiluminescence assay. AT P concentrations were significantly lower in embryos from -Cu dams that were cultured in -Cu serum than those removed from +Cu dams that were cultured in +Cu serum. These data support the concept that the teratogenicity of Cu deficiency occurs through a number of mechanisms including impairments in energy production and oxidant detente. The role of Cu deficiency-induced alterations in other processes such as angiogenesis and extracellular matrix maturation needs to be investigated.
UR - http://www.scopus.com/inward/record.url?scp=33750231647&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33750231647&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:33750231647
VL - 11
JO - FASEB Journal
JF - FASEB Journal
SN - 0892-6638
IS - 3
ER -