Cigarette smoke affects posttranslational modifications and inhibits capacitation-induced changes in human sperm proteins

• Physiological concentrations of CSE cause de-sumoylation of many sperm proteins.
• The decrease in sumoylation is not related to proteasome activity.
• CSE in the tubal fluid inhibits capacitation-associated protein phosphorylation.
• Exposure to tobacco of men and women can potentially cause fertility problems.

Sperm are highly dependent on posttranslational modifications of proteins. Massive phosphorylation on tyrosine residue is required for sperm capacitation. Sumoylation has also been recently implicated in spermatogenesis and sperm functions. Cigarette smoke is known to cause oxidative stress in different tissues, and several studies suggest that it causes oxidative stress in sperm. Whether tobacco affects posttranslational modifications in human sperm is currently unknown. In this study, we show that a short exposure of human sperm to physiological concentrations of cigarette smoke extract (CSE) causes the partial de-sumoylation of many sperm proteins. Furthermore, the presence of a low concentration of CSE in the human tubal fluid during an induction of in vitro capacitation inhibits the capacitation-associated increase in protein phosphorylation. Collectively, changes in posttranslational modifications may be one of the mechanisms through which exposure to tobacco can negatively affect sperm functions and cause fertility problems.