Piasecka M, Wenda-Rózewicka L, Kozanecka A, Rózewicki S, Laszczyńska M, Marchlewicz M
Katedry i Zakładu Histologii i Embriologii PAM.
Ginekol Pol. 1998 Jun;69(6):479-84.
To evaluate functional and ultrastructural alterations of the spermatozoa midpieces in patients with asthenozoospermia and to find a correlation between the damage of the midpieces and loss of sperm motility.
Routine, morphological assessment of the midpieces stained according to the Papanicolaou method, cytochemical study of the mitochondrial activity using reaction for the diaphorase/ NADH according to the Piasecka method and electron-microscopic investigation of the midpiece structures were performed.
The cytochemical reaction for diaphorase/NADH revealed disorders of the mitochondrial activity and subtle and drastic malformations in the spermatozoa midpieces. The unusually thickened midpieces contained the supernumerary mitochondria. In patients with severe asthenozoospermia, the damage of the accessory fibres and axonemal complex located in the midpiece, were obtained also.
This study indicates that mitochondrial defects are one of the causes that may account for loss of sperm motility in the population of patients.
评估弱精子症患者精子中段的功能和超微结构改变，并找出中段损伤与精子活力丧失之间的相关性。
对按照巴氏染色法染色的中段进行常规形态学评估，采用皮亚塞茨卡法通过黄递酶/NADH反应进行线粒体活性的细胞化学研究，并对中段结构进行电子显微镜检查。
黄递酶/NADH的细胞化学反应显示线粒体活性紊乱以及精子中段存在细微和严重畸形。异常增厚的中段含有多余的线粒体。在严重弱精子症患者中，还发现了位于中段的辅助纤维和轴丝复合体受损。
本研究表明线粒体缺陷是导致该患者群体精子活力丧失的原因之一。
