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通过将圆头人类精子注射到小鼠卵母细胞中分析其卵母细胞激活能力和染色体组成。

Analysis of the oocyte activating capacity and chromosomal complement of round-headed human spermatozoa by their injection into mouse oocytes.

作者信息

Rybouchkin A, Dozortsev D, Pelinck M J, De Sutter P, Dhont M

机构信息

Department of Gynaecology and Obstetrics, University Hospital, Ghent, Belgium.

出版信息

Hum Reprod. 1996 Oct;11(10):2170-5. doi: 10.1093/oxfordjournals.humrep.a019071.

Abstract

Intracytoplasmic sperm injection (ICSI) in the human is a very effective procedure which allows the fertilization of the majority of oocytes even in cases of extreme oligoasthenoteratozoospermia. Round-headed acrosomeless human spermatozoa, however, form an exception to this rule, because in about half of the couples with globozoospermia all oocytes remain unfertilized after injection. The incapacity of the spermatozoon to activate the oocyte following injection of round-headed spermatozoa could be the underlying mechanism. To investigate this hypothesis, activation rates of mouse oocytes injected with spermatozoa from a patient with globozoospermia were compared with those obtained after injection with normal spermatozoa. Of mouse oocytes surviving the injection with donor spermatozoa, 95% underwent activation, compared to none of the 88 mouse oocytes surviving the injection with round-headed spermatozoa. After fixation, prematurely condensed sperm chromosomes were found in these oocytes. Parthenogenetic activation of mouse oocytes (8% ethanol at 40 min after injection) injected with round-headed spermatozoa led to the activation of 96% of oocytes. These oocytes developed normally to the first mitosis and were fixed for analysis of the sperm karyotypes. The incidence of chromosomal abnormalities of round-headed spermatozoa (6%) was similar to that in spermatozoa from a fertile donor (9%). These data provide further information on the basic defect in cases of globozoospermia and demonstrate that globozoospermia is not associated with sperm karyotype abnormalities.

摘要

人类卵胞浆内单精子注射(ICSI)是一种非常有效的方法,即使在严重少弱畸精子症的情况下,也能使大多数卵母细胞受精。然而,圆头无顶体的人类精子是个例外,因为在大约一半的圆头精子症夫妇中,注射后所有卵母细胞都未受精。注射圆头精子后精子无法激活卵母细胞可能是其潜在机制。为了研究这一假设,将注射圆头精子症患者精子的小鼠卵母细胞激活率与注射正常精子后的激活率进行了比较。在注射供体精子后存活的小鼠卵母细胞中,95%发生了激活,而在注射圆头精子后存活的88个小鼠卵母细胞中,无一发生激活。固定后,在这些卵母细胞中发现了过早凝聚的精子染色体。用圆头精子注射的小鼠卵母细胞(注射后40分钟用8%乙醇)进行孤雌激活,导致96%的卵母细胞被激活。这些卵母细胞正常发育到第一次有丝分裂,并固定用于分析精子核型。圆头精子的染色体异常发生率(6%)与可育供体精子的发生率(9%)相似。这些数据为圆头精子症病例的基本缺陷提供了进一步信息,并表明圆头精子症与精子核型异常无关。

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