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

Citation
Ma. Jankowski-hennig et al., Zinc-deficient rat embryos have increased caspase 3-like activity and apoptosis, BIOC BIOP R, 271(1), 2000, pp. 250-256
Citations number
69
Categorie Soggetti
Biochemistry & Biophysics
Journal title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN journal
0006291X → ACNP
Volume
271
Issue
1
Year of publication
2000
Pages
250 - 256
Database
ISI
SICI code
0006-291X(20000429)271:1<250:ZREHIC>2.0.ZU;2-0
Abstract
Caspase activity is a hallmark of apoptosis. Given that maternal zinc (Zn) deficiency results in apoptosis in the rat embryo, we assessed caspase acti vity in Zn-deficient embryos. Mid-gestation rat embryos were collected from dams fed either a Zn-deficient (0.5 mu g Zn/g) diet ad libitum, or a Zn-ad equate (25 mu g Zn/g) diet ad libitum or pair fed to dams fed the Zn-defici ent 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 eithe r increased or normal levels of cell death. Zn-deficient embryos displaying increased cell death had increased caspase activity. Embryos with normal l evels of cell death, regardless of maternal diet, had similar caspase activ ities. Thus, Zn-deficiency-induced apoptosis in vivo is associated with inc reased caspase activity, (C) 2000 Academic Press.