Abstract
The female reproductive system represents a sensitive target of the harmful effects of cigarette smoke, with folliculogenesis as one of the ovarian processes most affected by this exposure. The aim of this study was to analyze the impact of tobacco smoking on expression of oxidative stress-related genes in cumulus cells (CCs) from smoking and non-smoking women undergoing IVF techniques. Real time PCR technology was used to analyze the gene expression profile of 88 oxidative stress genes enclosed in a 96-well plate array. Statistical significance was assessed by one-way ANOVA. The biological functions and networks/pathways of modulated genes were evidenced by ingenuity pathway analysis software. Promoter methylation analysis was performed by pyrosequencing. Our results showed a down-regulation of 24 genes and an up-regulation of 2 genes (IL6 and SOD2, respectively) involved in defense against oxidative damage, cell cycle regulation, as well as inflammation in CCs from smoking women. IL-6 lower promoter methylation was found in CCs of the smokers group. In conclusion, the disclosed overall downregulation suggests an oxidant-antioxidant imbalance in CCs triggered by cigarette smoking exposure. This evidence adds a piece to the puzzle of the molecular basis of female reproduction and could help underlay the importance of antioxidant treatments for smoking women undergoing IVF protocols.
Highlights
The data presented in this study provides evidence pacity may result in a condition called oxidative stress
In the last five decades a significant trend towards a progressive worldwide decline in human fertility has been reported in the international literature; much attention has been placed on identifying environmental and lifestyle modifiable risk factors that affect human reproductive function [81]
Several differentially expressed key molecular genes related to oxidative stress and the apoptotic pathway were identified in cumulus cells (CCs) following prolonged exposure to cigarette smoke
Summary
The male and female reproductive systems represent sensitive targets of the harmful effects of cigarette smoke [3,4,5]. Cigarette smoke exposure is associated with earlier menopause and delayed conception [6]. The ovaries are highly vulnerable to the deranging effects of cigarette smoking; steroidogenesis and folliculogenesis are the ovarian processes most affected by this exposure [4,5]. The cigarette smoke-induced oxidative stress (OS) appears to be one of the main causes of ovarian injury [12,13,14], together with the abnormal crosstalk between oocyte and granulosa-cells, DNA damage and increased cell death [2,4,5,15]. The presence of ROS at low concentrations exerts a physiological role for cell homeostasis
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