Tobacco-induced microRNAs profile alterations in human spermatozoa: a preliminary study for further knowledge of toxical spermatogenesis impairment. Homo sapiens

Tobacco smoking generates deleterious effects on human semen quality but mechanisms by which cigarettes smoking can impact spermatogenesis are poorly understood. Recent works have shown that spermatozoa RNAs can be used to understand mechanisms involved in tobacco induced spermatogenesis impairment. We performed a prospective study of 8 smoker and 8 non-smoker patients in an university hospital. All patients were selected according to an occupational exposure standardized questionnaire and the sperm parameters. We performed gene expression and miRNA microarrays using RNA extracts from spermatozoa of 8 smokers and 8 non-smokers. Quantification of selected miRNA was performed using quantitative RT-PCR. We show that 16 genes were differentially expressed between smokers and non-smokers, of which 5 were upregulated and 11 were down regulated in smokers. 23 microRNAs were differentially expressed, of which 16 were upregulated and 7 were down regulated in smokers. Quantitative RT-PCR confirmed the down regulation in smokers for 3 microRNAs. Moreover in smokers, one of the upregulated genes is a putative target for one down regulated microRNA. This is a preliminary and innovating study on spermatozoa RNA extracts in the field of infertility. This preliminary study shows that large scale approaches are non invasive diagnostic tools that may help elucidate the mechanisms that mediate the response to tobacco smoke exposure on human spermatogenesis. This could be used to design biomarkers of human spermatogenetic damage, and help elucidate the fine regulatory mechanisms that mediate responses to environmental agent exposure during human spermatogenesis. Overall design: miRNAs were extracted from spermatozoa of 8 patients including: 4 non-smokers and 4 smokers