EXPRESSION OF SUPEROXIDE-DISMUTASE, CATALASE AND GLUTATHIONE-PEROXIDASE IN THE BOVINE CORPUS-LUTEUM - EVIDENCE SUPPORTING A ROLE FOR OXIDATIVE STRESS IN LUTEOLYSIS

Citation
Br. Rueda et al., EXPRESSION OF SUPEROXIDE-DISMUTASE, CATALASE AND GLUTATHIONE-PEROXIDASE IN THE BOVINE CORPUS-LUTEUM - EVIDENCE SUPPORTING A ROLE FOR OXIDATIVE STRESS IN LUTEOLYSIS, Endocrine, 3(3), 1995, pp. 227-232
Citations number
35
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
1355008X
Volume
3
Issue
3
Year of publication
1995
Pages
227 - 232
Database
ISI
SICI code
1355-008X(1995)3:3<227:EOSCAG>2.0.ZU;2-V
Abstract
Apoptosis, a type of physiological or active cell death, has been impl icated as a mechanism underlying regression of the corpus luteum (CL) in the rat, bovine, rabbit and ovine ovary. Previous in vitro studies of cultured luteal cells have also provided evidence which suggests th at reactive oxygen species play an important role in luteolysis in the rodent ovary. To further evaluate the potential role of oxidative str ess in luteal cell demise, changes in the expression of several enzyme s known to protect cells from oxidative stress were investigated using bovine CL collected from ovaries of non-pregnant (day 21 of the estro us cycle; regressed CL) and pregnant (day 21 of pregnancy; functional CL) animals. Biochemical analysis of genomic DNA extracted from these two pools of CL demonstrated the presence of extensive levels of inter nucleosomal DNA cleavage characteristic of cell death via apoptosis in regressed, but not in functional, CL. Northern blot analysis of total RNA indicated that functional CL expressed significantly higher level s of mRNA encoding secreted superoxide dismutase (SEC-SOD, 1.9 kb) and manganese-containing or mitochondrial SOD (Mn-SOD, multiple transcrip ts) as compared to regressed CL. Similarly, levels of mRNA encoding ca talase (2.1 kb), an enzyme responsible for detoxification of peroxides to water, were significantly higher in functional versus regressed CL . From these data, we conclude that a decline in expression of specifi c oxidative response genes occurs during luteolysis, and that maintain ed expression of these genes in the CL during pregnancy may prevent ox idative damage and delay regression.