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Blood cell mitochondrial DNA content and premature ovarian aging

Primary ovarian insufficiency (POI) is a critical fertility defect characterized by an anticipated and silent impairment of the follicular reserve, but its pathogenesis is largely unexplained. The frequent maternal inheritance of POI together with a remarkable dependence of ovarian folliculogenesis...

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Bibliographic Details
Published in:PloS one 2012-08, Vol.7 (8), p.e42423-e42423
Main Authors: Bonomi, Marco, Somigliana, Edgardo, Cacciatore, Chiara, Busnelli, Marta, Rossetti, Raffaella, Bonetti, Silvia, Paffoni, Alessio, Mari, Daniela, Ragni, Guido, Persani, Luca
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Language:English
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Summary:Primary ovarian insufficiency (POI) is a critical fertility defect characterized by an anticipated and silent impairment of the follicular reserve, but its pathogenesis is largely unexplained. The frequent maternal inheritance of POI together with a remarkable dependence of ovarian folliculogenesis upon mitochondrial biogenesis and bioenergetics suggested the possible involvement of a generalized mitochondrial defect. Here, we verified the existence of a significant correlation between blood and ovarian mitochondrial DNA (mtDNA) content in a group of women undergoing ovarian hyperstimulation (OH), and then aimed to verify whether mtDNA content was significantly altered in the blood cells of POI women. We recruited 101 women with an impaired ovarian reserve: 59 women with premature ovarian failure (POF) and 42 poor responders (PR) to OH. A Taqman copy number assay revealed a significant mtDNA depletion (P
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0042423