Protein profile screening: Reduced expression of Sord in the mouse epididymis induced by nicotine inhibits tyrosine phosphorylation level in capacitated spermatozoa

Jingbo Dai, Wangjie Xu, Xianglong Zhao, Meixing Zhang, Dong Zhang, Dongsheng Nie, Min Bao, Zhaoxia Wang, Lianyun Wang, Zhongdong Qiao*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Many studies have revealed the hazardous effects of cigarette smoking and nicotine exposure on male fertility, but the actual, underlying molecular mechanism remains relatively unclear. To evaluate the detrimental effects of nicotine exposure on the sperm maturation process, two-dimensional gel electrophoresis and mass spectrometry analyses were performed to screen and identify differentially expressed proteins from the epididymal tissue of mice exposed to nicotine. Data mining analysis indicated that 15 identified proteins were mainly involved in the molecular transportation process and the polyol pathway, indicating impaired epididymal secretory functions. Experiments in vitro confirmed that nicotine inhibited tyrosine phosphorylation levels in capacitated spermatozoa via the downregulated seminal fructose concentration. Sord, a key gene encoding sorbitol dehydrogenase, was further investigated to reveal that nicotine induced hyper-methylation of the promoter region of this gene. Nicotine-induced reduced expression of Sord could be involved in impaired secretory functions of the epididymis and thus prevent the sperm from undergoing proper maturation and capacitation, although further experiments are needed to confirm this hypothesis.

Original languageEnglish (US)
Pages (from-to)227-237
Number of pages11
JournalReproduction
Volume151
Issue number3
DOIs
StatePublished - Mar 2016

ASJC Scopus subject areas

  • Embryology
  • Reproductive Medicine
  • Endocrinology
  • Obstetrics and Gynecology
  • Cell Biology

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