据香港中通社报道，香港中文大学研究人员在精子里发现一个上皮细胞离子信道，可能影响男性生育能力。他们之前的研究证明，同样的离子信道表达于女性生殖道，如果有功能缺陷，会导致女性不育。
这项新的研究结果已在线刊于权威学术期刊美国科学院院刊。
精子必须经过一个启动的过程才能使卵子受精，这过程称为精子获能。这个精子获能的过程已知是由碳酸氢盐诱发。由陈小章教授领导的香港中文大学上皮细胞生物学研究中心的研究人员，与浙江医学科学院合作，证实囊性纤维化跨膜电导调节器(CFTR)负责输送碳酸氢根进入精子，对精子授精能力及男性生育能力非常重要。
CFTR是一个阴离子信道，其基因突变会导致囊性纤维化，因为氯离子和碳酸氢根(HCO3-)分泌缺陷，引发一系列器官病征。
香港中文大学上皮细胞生物学研究中心较早的研究已证实CFTR存在于女性生殖道上，其功能失效可阻止精子在女性生殖道内的获能。
百分之九十五患上囊性纤维化的男性病人，因先天性无输精管而不育，但囊性纤维化跨膜电导调节器基因突变会否导致其它类型的男性不育，仍有争议。研究人员首次在人类和老鼠的精子发现CFTR。CFTR抑制剂或抗体能有效减低精子获能，及相关的碳酸氢根依赖反应；研究人员又证实CFTR突变老鼠，其精子授精能力大大比野生型老鼠为低。
研究结果显示，精子的CFTR功能为碳酸氢根的传输，促使精子获能；而CFTR基因突变引致功能失效，会降低精子授精能力，这是先天性无输精管以外另一导致男性不育的可能因素。
研究同时显示，CFTR缺陷可以对男性不育造成不同程度的影响，目前已知的与CFTR相关的基因突变逾二千种，研究结果可能为许多未明原因的男性不育个案提供新的解释，并提供诊断的新靶子。
原始出处:
PNAS Published online before print May 22, 2007
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0609253104
Medical Sciences
Cystic fibrosis transmembrane conductance regulator is vital to sperm fertilizing capacity and male fertility
( bicarbonate | CFTR | sperm capacitation )
Wen Ming Xu *, Qi Xian Shi , Wen Ying Chen *, Chen Xi Zhou *, Ya Ni , Dewi Kenneth Rowlands *, Guo Yi Liu , Hu Zhu *, Ze Gang Ma *, Xiao Fei Wang , Zhang Hui Chen , Si Chang Zhou , Hong Shan Dong *, Xiao Hu Zhang *, Yiu Wa Chung *, Yu Ying Yuan , Wan Xi Yang , and Hsiao Chang Chan *¶
*Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Sciences, Department of Physiology, Faculty of Medicine, Chinese University of Hong Kong, Shatin, NT, Hong Kong, China; Zhejiang Academy of Medical Sciences, Hangzhou 310013, China; Zhejiang University School of Medicine, College of Life Sciences, Hangzhou 310058, China; and Department of Physiology, Harbin Medical University, Harbin 150086, China
Edited by Ryuzo Yanagimachi, University of Hawaii, Honolulu, HI, and approved April 16, 2007 (received for review October 23, 2006)
Abstract
Cystic fibrosis transmembrane conductance regulator (CFTR) is an anion channel, mutations of which cause cystic fibrosis, a disease characterized by defective Cl- and HCO3- transport. Although >95% of all CF male patients are infertile because of congenital bilateral absence of the vas deferens (CBAVD), the question whether CFTR mutations are involved in other forms of male infertility is under intense debates. Here we report that CFTR is detected in both human and mouse sperm. CFTR inhibitor or antibody significantly reduces the sperm capacitation, and the associated HCO3--dependent events, including increases in intracellular pH, cAMP production and membrane hyperpolarization. The fertilizing capacity of the sperm obtained from heterozygous CFTR mutant mice is also significantly lower compared with that of the wild-type. These results suggest that CFTR in sperm may be involved in the transport of HCO3- important for sperm capacitation and that CFTR mutations with impaired CFTR function may lead to reduced sperm fertilizing capacity and male infertility other than CBAVD.
