Yunes Roberto, Doncel Gustavo F, Acosta Anibal A
Jones Institute for Reproductive Medicine, Department of Obstetrics and Gynecology, Eastern Virginia Medical School, Norfolk, VA, USA.
Biocell. 2003 Apr;27(1):29-36.
Our objective was to study the incidence of sperm-tail phosphotyrosine immunoreactivity in normozoospermic and asthenozoospermic human sperm samples, its association with sperm motion parameters, particularly hyperactivated motility, and its potential involvement in the pathogenesis of asthenozoospermia. The work was conducted as a prospective experimental study in the Sperm Biology and Andrology laboratories of the Jones Institute, a medical school-based fertility center. The study subjects were healthy fertile male donors (normozoospermic samples) and infertile patients (asthenozoospermic samples) attending the center. Recently ejaculated semen samples were washed twice to eliminate seminal plasma and a swim-up was performed to select the motile population which, in turn, was incubated up to 18 h at 37 degrees C in 3.5% human serum albumin-supplemented Ham's F10 to allow for capacitation. For evaluation, sperm aliquots were taken pre-swim-up (T0), immediately post swim-up (T1), at 6 h (T6), and 18 h (T18) of incubation. The main outcome measures were computer-analyzed sperm motion parameters and hyperactivated motility, and immunodetection of phosphotyrosine (PY)-containing proteins. During the capacitating incubation, normozoospermic samples displayed maximum motility, velocity, and hyperactivation at T6, significantly decreasing their values at T18. PY-proteins were located both at the tail and head of spermatozoa. Their expression increased progressively during the incubation, being present in about 70% of the sperm tails at T18. Asthenozoospermic samples showed an inability to respond to capacitation with an increase in motion parameters and PY-phosphorylation. At T6, both hyperactivation and PY-phosphorylation were significantly lower than in normal samples. Our results suggest that PY-phosphorylation of tail proteins is highly conspicuous in human spermatozoa, and increases its incidence in a time-dependent manner, as more sperm become capacitated. Asthenozoospermic samples displaying low percentages of motile sperm and altered motion characteristics showed a decreased incidence of PY-phosphorelated sperm. Tail protein PY-phosphorylation may be related to sperm movement, especially to hyperactivated motility and its deficiency may be associated to asthenozoospermia.
我们的目的是研究正常精子症和弱精子症患者精液样本中精子尾部磷酸化酪氨酸免疫反应性的发生率,其与精子运动参数(尤其是超活化运动)的关系,以及其在弱精子症发病机制中的潜在作用。本研究是在琼斯研究所的精子生物学和男科学实验室进行的一项前瞻性实验研究,该研究所是一个以医学院为基础的生育中心。研究对象为到该中心就诊的健康有生育能力的男性捐赠者(正常精子症样本)和不育患者(弱精子症样本)。近期射出的精液样本经两次洗涤以去除精浆,然后进行上游法以选择活动精子群体,这些精子继而在37℃下于补充了3.5%人血清白蛋白的哈姆F10培养基中孵育18小时以使其获能。为进行评估,在孵育前(T0)、上游法后即刻(T1)、孵育6小时(T6)和18小时(T18)时采集精子样本。主要观察指标为计算机分析的精子运动参数和超活化运动,以及含磷酸化酪氨酸(PY)蛋白的免疫检测。在获能孵育过程中,正常精子症样本在T6时表现出最大运动性、速度和超活化,在T18时其值显著降低。PY蛋白位于精子的尾部和头部。其表达在孵育过程中逐渐增加,在T18时约70%的精子尾部有表达。弱精子症样本表现出对获能无反应,运动参数和PY磷酸化无增加。在T6时,超活化和PY磷酸化均显著低于正常样本。我们的结果表明,精子尾部蛋白的PY磷酸化在人类精子中非常明显,并随时间呈依赖性增加,因为更多精子获能。弱精子症样本中活动精子百分比低且运动特征改变,显示PY磷酸化精子的发生率降低。尾部蛋白PY磷酸化可能与精子运动有关,尤其是与超活化运动有关,其缺乏可能与弱精子症相关。