TY - JOUR
T1 - Expression of Copper/Zinc superoxide dismutase and glutathione peroxidase in organs of developing mouse embryos, fetuses, and neonates
AU - De Haan, Judy B.
AU - Tymms, Martin J.
AU - Cristiano, Francesca
AU - Kola, Ismail
PY - 1994/2
Y1 - 1994/2
N2 - The rise in antioxidant enzyme activity in the lungs of late-gestation fetuses is thought to be caused by the preparation of the pulmonary antioxidant system for birth. However, recent data have shown that such a rise also occurs in the livers of late-gestation fetuses. Consequently, this surge cannot solely be ascribed to the preparation of the pulmonary antioxidant system for birth. In this study we examine the expression of copper/zinc superoxide dismutase (Sod1) and glutathione peroxidase (Gpx1) in various organs of late-gestational mouse fetuses. Furthermore, we compare the expression of these genes in organs of fetuses, neonates, and adult mice. These studies were carried out to investigate whether the change in mRNA levels for these two genes is related to a developmental change in oxidant stress. Our data demonstrate that an increase in both Sod1 and Gpx1 mRNA occurs in lungs and livers of late-gestational mouse fetuses. The brain demonstrates an increase in Sod1 expression at or around the time of birth, the kidney shows an elevation in Gpx1 mRNA levels, and the heart fails to demonstrate a surge in both Sod1 and Gpx1 mRNA levels. Our data show that the liver is the organ with the highest levels of Sod1 and Gpx1 mRNA in embryos and neonates (immediately after birth). In the adult, the liver has the highest levels of Sod1 mRNA and the spleen the highest level of Gpx1 mRNA. These data suggest that the levels of Sod1 and Gpx1 mRNA are unrelated to oxygen consumption and to oxygen tension exposure of individual organs and do not necessarily appear to occur in the lung solely in preparation for birth. The reasons for the increase in antioxidant enzyme(s) mRNA levels in late gestation are more complex and may involve other factors.
AB - The rise in antioxidant enzyme activity in the lungs of late-gestation fetuses is thought to be caused by the preparation of the pulmonary antioxidant system for birth. However, recent data have shown that such a rise also occurs in the livers of late-gestation fetuses. Consequently, this surge cannot solely be ascribed to the preparation of the pulmonary antioxidant system for birth. In this study we examine the expression of copper/zinc superoxide dismutase (Sod1) and glutathione peroxidase (Gpx1) in various organs of late-gestational mouse fetuses. Furthermore, we compare the expression of these genes in organs of fetuses, neonates, and adult mice. These studies were carried out to investigate whether the change in mRNA levels for these two genes is related to a developmental change in oxidant stress. Our data demonstrate that an increase in both Sod1 and Gpx1 mRNA occurs in lungs and livers of late-gestational mouse fetuses. The brain demonstrates an increase in Sod1 expression at or around the time of birth, the kidney shows an elevation in Gpx1 mRNA levels, and the heart fails to demonstrate a surge in both Sod1 and Gpx1 mRNA levels. Our data show that the liver is the organ with the highest levels of Sod1 and Gpx1 mRNA in embryos and neonates (immediately after birth). In the adult, the liver has the highest levels of Sod1 mRNA and the spleen the highest level of Gpx1 mRNA. These data suggest that the levels of Sod1 and Gpx1 mRNA are unrelated to oxygen consumption and to oxygen tension exposure of individual organs and do not necessarily appear to occur in the lung solely in preparation for birth. The reasons for the increase in antioxidant enzyme(s) mRNA levels in late gestation are more complex and may involve other factors.
UR - http://www.scopus.com/inward/record.url?scp=0027955869&partnerID=8YFLogxK
U2 - 10.1203/00006450-199402000-00013
DO - 10.1203/00006450-199402000-00013
M3 - Article
C2 - 8165054
AN - SCOPUS:0027955869
SN - 0031-3998
VL - 35
SP - 188
EP - 196
JO - Pediatric Research
JF - Pediatric Research
IS - 2
ER -