Zinc-deficient rat embryos have increased caspase 3-like activity and apoptosis.
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 Zn/g) diet ad libitum, or a Zn-adequate (25 microg 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.
Jankowski-Hennig
M A
MA
Department of Nutrition, University of California, Davis, California 95616, USA.
Clegg
M S
MS
Daston
G P
GP
Rogers
J M
JM
Keen
C L
CL
D000818:Animals; D017209:Apoptosis; D001835:Body Weight; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism*; D004622:Embryo, Mammalian / Q000201:enzymology* / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D015032:Zinc / Q000172:deficiency* / Q000502:physiology
C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases; D015032:Zinc