精子无力症
精子活力
精子
生物
运动性
男科
精液
人口
男性不育
不育
医学
解剖
遗传学
怀孕
环境卫生
作者
Fiore Pelliccione,Alessandro Micillo,Giuliana Cordeschi,Anatolia D’Angeli,Stefano Necozione,L. Gandini,Andrea Lenzi,Felice Francavilla,Sandro Francavilla
标识
DOI:10.1016/j.fertnstert.2010.07.1086
摘要
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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