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This Article Full Text Full Text (PDF) All Versions of this Article: 289/6/E1101    most recent 00223.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Navarro, A. Articles by Boveris, A. Search for Related Content PubMed PubMed Citation Articles by Navarro, A. Articles by Boveris, A.

Mitochondrial function and mitochondria-induced apoptosis in an overstimulated rat ovarian cycle

¹Department of Biochemistry and Molecular Biology and ²Department of Obstetrics and Gynecology, University Hospital of Puerto Real; ³Department of Cell Biology and Histology, School of Medicine, University of Cádiz, Cadiz, Spain; and ⁴School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina

Submitted 16 May 2005 ; accepted in final form 3 July 2005

Female rats were treated with FSH (40 IU/kg) on the first and second diestrus days (D1 and D2) and with LH (40 IU/kg) on 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 mitochondrial nitric oxide synthase (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 thiobarbituric acid-reactive substances and protein carbonyls, indicates 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.

ovarian follicle; oxygen uptake; mitochondrial nitric oxide synthase; respiratory chain; oxidative damage

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