Menstruation Research Today is a free monthly online journal that collates and summarizes the latest research about Menstruation, including details on menstrual cycle, pregnancy, pain, irregular menstruation. | ||||||||
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Mitochondrial function and mitochondria-induced apoptosis in an overstimulated rat ovarian cycle.Navarro A, Torrejón R, Bández MJ, López-Cepero JM, Boveris A Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, University Hospital of Puerto Real, Plaza Fragela 9, 11003 Cádiz, Spain. ana.navarro@uca.es 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 O(2)(-) and H(2)O(2) appear well adapted to serve the proliferation-apoptosis sequence of the ovarian cycle. Published 10 November 2005 in Am J Physiol Endocrinol Metab, 289(6): E1101-9.
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