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1 Department of Biochemistry and Molecular Biology, School of Medicine, University of Cadiz, Cadiz, Spain
2 Department of Obstetric and Gynecology University Hospital of Puerto Real, School of Medicine, University of Cadiz, Cadiz, Spain
3 Department of Cell Biology and Histology, School of Medicine, University of Cadiz, Cadiz, Spain
* To whom correspondence should be addressed. E-mail: ana.navarro{at}uca.es.
Female rats were treated with FSH (40 IU/kg) in the first and second diestrus day (D1 and D2) and with LH (40 IU/kg) in the proestrus (P) day to synchronize and maximize ovarian changes. Follicle area increased by 50 % from D1 to P and the estrus (E) phase showed multiple corpora lutea and massive apoptosis. Increased oxygen uptakes (42-102 %) were determined in ovary slices and in isolated mitochondria in active state 3 along the proliferation phase (D1-D2-P) that returned to initial values in the E phase. Mitochondrial content and the electron transfer activities of complexes I and IV were also maximal in the P phase (20-79 % higher than in D1). Production of NO by mtNOS, biochemically determined, and the mtNOS functional activity in regulating state 3 oxygen uptake were also maximal at P and 79-88 % higher than at D1. The moderately increased rate of NO in the proliferative phase is associated with mitochondrial biogenesis whereas the high rate of NO generation by mtNOS at phase P appears to trigger mitochondria-dependent apoptosis. The calculated fraction of ovary mitochondria in state 3 was at a minimal value at the P phase. Mitochondrial oxidative damage, with increased TBARS and protein carbonyls, indicate progressive mitochondrial dysfunction between phases P and E. The roles of mitochondria as ATP-provider, as a source of NO to signal for mitochondrial proliferation and mitochondria-dependent apoptosis, and as a source of O2- and H2O2 appear well adapted to serve the proliferation-apoptosis sequence of the ovarian cycle.
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