Zinc-deficient rat embryos have increased caspase 3-like activity and apoptosis

Margaret A. Jankowski-Hennig, Michael S. Clegg, George P. Daston, John M. Rogers, Carl L Keen

Research output: Contribution to journalArticlepeer-review

56 Scopus citations


Caspase activity is a hallmark of apoptosis. Given that maternal zinc (Zn) deficiency results in apoptosis in the rat embryo, we assessed caspase activity in Zn-deficient embryos. Mid-gestation rat embryos were collected from dams fed either a Zn-deficient (0.5 μg Zn/g) diet ad libitum, or a Zn-adequate (25 μg Zn/g) diet ad libitum or pair fed to dams fed the Zn-deficient diet. Embryos from dams fed the Zn-adequate diet had a normal level of cell death, while embryos from the dams fed the Zn-deficient diet had either increased or normal levels of cell death. Zn-deficient embryos displaying increased cell death had increased caspase activity. Embryos with normal levels of cell death, regardless of maternal diet, had similar caspase activities. Thus, Zn-deficiency-induced apoptosis in vivo is associated with increased caspase activity. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)250-256
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - Apr 29 2000


  • Apoptosis
  • Caspase 3
  • Cell death
  • Deficiency
  • Development
  • Embryo
  • Pregnancy
  • Zinc

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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