ABSTRACT
The aim of the present study was to evaluate consequences of cigarette smoking on male gametes. In this prospective study, sperm parameters such as sperm density, motility, viability and normal morphology were measured according to the WHO criteria. In addition to these standard parameters, we analysed the degree of DNA fragmentation in spermatozoa using the TUNEL-assay with flow cytometry detection in 57 non-smokers and 51 smokers seeking for infertility counselling. The smoking intoxication was assessed by questionnaire and measured with the CO-Tester. We show that smokers' spermatozoa have a significantly higher DNA fragmentation than non-smokers (32% versus 25.9%, p<0.01). In contrast there is no significant difference in conventional parameters between smokers and non-smokers. The degree of sperm DNA fragmentation is not significantly correlated with any of the conventional parameters. These findings suggest that cigarette smoking may have deleterious effects on sperm nuclear quality and that sperm DNA fragmentation can therefore be considered as an independent parameter with diagnostic, prognostic, and strategic value in the treatment of infertility.
Subject(s)
DNA Fragmentation , Smoking/pathology , Spermatozoa/pathology , Adult , Cross-Sectional Studies , Humans , In Situ Nick-End Labeling , Infertility, Male/etiology , Male , Prospective Studies , Smoking/adverse effects , Sperm Count , Sperm MotilityABSTRACT
In vitro studies were designed to determine whether Sertoli cell-delivered ABP could act on spermatogenetic events, whether such an action could occur via a paracrine or a juxtacrine pathway and whether sex steroids could be involved in this action. ABP delivery to germ cells was achieved using an in vitro model based on recombinant rat ABP-producing mouse Sertoli cells cocultivated with rat spermatids. Using semi-quantitative RT-PCR, the expression of the Tnp 1 gene encoding the Transition Protein 1, involved in the histone to protamine replacement during spermatid nuclear transformation, was analyzed. Our results provide clear evidence that Sertoli cell-derived ABP acts on spermatids by modifying the TP1 mRNA level. This outcome, strictly requiring juxtacrine conditions, is obtained in the absence of sex steroid hormones. To our knowledge this is the first evidence of an effect of ABP itself on male germ cells.
