Altered ultrastructure of mitochondrial membranes is strongly associated with unexplained asthenozoospermia  

Oleh:

Pelliccione, F. ; Micillo, Alessandro ; Cordeschi, Giuliana ; D’Angeli, Anatolia ; Necozione, Stefano ; Gandini, Loredana ; Lenzi, Andrea ; Francavilla, Felice ; Francavilla, Sandro

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 95 no. 02 (Feb. 2011), page 641-646 .
Topik: SPERMATOZOA; Asthenozoospermia; sperm ultrastructure; sperm tail middle piece; mitochondria

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2011.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Objective To explore the contribution of an altered structure of sperm mitochondria to human asthenozoospermia. Design A retrospective study. Setting Andrology Clinic, University of L’Aquila. Patient(s) Fifteen ejaculates with forward motility (FM) =50%, and 57 asthenozoospermic ejaculates (FM <50%, sperm vitality >50%), including 14 ejaculates with systematic genetic defects of tail principal piece, and 43 ejaculates with unexplained asthenozoospermia. Intervention(s) Fifty sections of tail middle piece (MP) were blindly analyzed by transmission electron microscopy in each ejaculate for normal mitochondrial membrane organization, after exclusion of tails with disrupted cell membranes. Main Outcome Measure(s) Percentage of MPs with normal mitochondrial membranes (% normal MPs). Result(s) Percent normal MPs showed a strong correlation with forward motility. Variation of % normal MPs explained a 45% variation of sperm motility at multivariate linear regression analysis, confirming the strong association between the two parameters in a population including ejaculates with normal motility and with unexplained asthenozoospermia. Percent normal MPs was significantly reduced in severe unexplained asthenozoospermia (FM <10%; n = 16) compared with samples with normal motility (FM =50%; n = 15); 21% (10.5%–38%) and 68% (52%–73%), respectively. Conclusion(s) Structural defects in mitochondrial membranes represent a main feature of severe unexplained asthenozoospermia.

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