Spatial and Temporal Ontogenies of Glutathione Peroxidase and Glutathione Disulfide Reductase During Development of the Prenatal Rat

✍ Scribed by Hyungsuk Choe; Jason M. Hansen; Craig Harris

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 255 KB
• Volume: 15
• Category: Article
• ISSN: 1095-6670
• DOI: 10.1002/jbt.17

✦ Synopsis

Abstract

Spatial and temporal expression and regulation of the antioxidant enzymes, glutathione peroxidase
(GSH‐Px), glutathione disulfide reductase (GSSG‐Rd) may be important in determining cell‐specific
susceptibility to embryotoxicants. Creation of tissue‐specific ontogenies for antioxidant enzyme activities during development is
an important first step in understanding regulatory relationships. Early organogenesis‐stage embryos were grouped
according to the somite number (GD 9–13), and fetuses were evaluated by gestational day (GD 14–21). GSH‐Px activities in the
visceral yolk sac (VYS) increased on consecutive days from GD 9 to GD 13, representing a 5.7‐fold increase during this period of development. GSH‐Px
activities in VYS decreased after GD 13, ultimately constituting a 37% decrease at GD 21. Head, heart, and trunk specific activities generally
increased from GD 9 to GD 13 albeit not to the same magnitude as detected in the VYS. GSSG‐Rd activities showed substantial increases in the VYS from GD 9 to GD
13, 6.3‐fold and decreased thereafter to 50% by GD 21. The greatest changes in enzyme activities were noted in the period between GD 10 and GD 11,
where the embryo establishes an active cardiovascular system and begins to convert to aerobic metabolism. Generally, from GD 14–21, embryonic organ
GSH‐Px and GSSG‐Rd activities either remained constant or increased as gestation progressed. These studies suggest the importance of the VYS in dealing with
ROS and protecting the embryo. Furthermore, understanding the consequences of lower antioxidant activities during organogenesis may help to pinpoint periods of
teratogenic susceptibility to xenobiotics and increased oxygen. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:197–206, 2001