Cigarette smoking increased seminal plasma cholesterol levels and significantly reduced intracellular sperm calcium in samples from infertile males

Abstract

OBJECTIVE: Cigarette smoking is one of the most common toxic habits that are able to induce deleterious effects on gametes and has been associated with an increase in oxidative stress within the ejaculates. We are previously demonstrated that smoking is negatively affecting intracellular antioxidant enzymes. Also, it could be interesting to study other molecular changes on sperm. Intracellular concentrations of calcium ([Ca+2]) and cholesterol ([CH]) in the sperm membrane has been demonstrated to be important markers of the sperm quality due to its direct relationship with sperm morphology and fertility potential; and mitochondrial activity (MA) is strongly related with sperm motility. Our aim with this study was to correlate levels of Ca+2, CH and MA with the cigarette consumption (CC).DESIGN: Prospective cohort study on 135 semen samples from infertile males.MATERIALS AND METHODS: Two groups were established according to CC: non-smoking (n=73) and smoking males (n=62). Patients with recent fever, exposure to gonadotoxins or heavy metals, and those with alcohol and/or drug consumption in the previous 3 months were excluded. T test was employed to detect significant differences. Basic sperm parameters were analyzed; [Ca+2] and [CH] on seminal plasma were determined by enzymoimmunoanalysis. Intracellular [Ca+2] and [CH] in the sperm membrane and MA, were determined by fluorometry.RESULTS: There was no correlation between standard seminal parameters and CC; [CH] on seminal plasma in smokers was higher than in non smokers (p=0.044). However, sperm plasma membrane [CH] between smokers and non smokers had not significant differences. Seminal plasma Ca+2 had not significant differences between groups, but intracellular Ca+2 in smokers resulted significantly diminished when where compared with non smokers (p=0.030). The MA present in smokers and non smokers was not different.CONCLUSIONS: We have observed a significant increase of CH levels in seminal plasma from smokers (as described in smoker's blood); but not on sperm membrane; probably preserving the capacitation function in which CH has been implicated. We have also demonstrated that smoking is negatively affecting intracellular sperm Ca+2, and this phenomenon should produce important changes in the cellular physiology of those sperm cells from infertile male smokers, although their mitochondrias were not altered. Further research is needed to study the potential negative effects of cigarette on gametes. OBJECTIVE: Cigarette smoking is one of the most common toxic habits that are able to induce deleterious effects on gametes and has been associated with an increase in oxidative stress within the ejaculates. We are previously demonstrated that smoking is negatively affecting intracellular antioxidant enzymes. Also, it could be interesting to study other molecular changes on sperm. Intracellular concentrations of calcium ([Ca+2]) and cholesterol ([CH]) in the sperm membrane has been demonstrated to be important markers of the sperm quality due to its direct relationship with sperm morphology and fertility potential; and mitochondrial activity (MA) is strongly related with sperm motility. Our aim with this study was to correlate levels of Ca+2, CH and MA with the cigarette consumption (CC). DESIGN: Prospective cohort study on 135 semen samples from infertile males. MATERIALS AND METHODS: Two groups were established according to CC: non-smoking (n=73) and smoking males (n=62). Patients with recent fever, exposure to gonadotoxins or heavy metals, and those with alcohol and/or drug consumption in the previous 3 months were excluded. T test was employed to detect significant differences. Basic sperm parameters were analyzed; [Ca+2] and [CH] on seminal plasma were determined by enzymoimmunoanalysis. Intracellular [Ca+2] and [CH] in the sperm membrane and MA, were determined by fluorometry. RESULTS: There was no correlation between standard seminal parameters and CC; [CH] on seminal plasma in smokers was higher than in non smokers (p=0.044). However, sperm plasma membrane [CH] between smokers and non smokers had not significant differences. Seminal plasma Ca+2 had not significant differences between groups, but intracellular Ca+2 in smokers resulted significantly diminished when where compared with non smokers (p=0.030). The MA present in smokers and non smokers was not different. CONCLUSIONS: We have observed a significant increase of CH levels in seminal plasma from smokers (as described in smoker's blood); but not on sperm membrane; probably preserving the capacitation function in which CH has been implicated. We have also demonstrated that smoking is negatively affecting intracellular sperm Ca+2, and this phenomenon should produce important changes in the cellular physiology of those sperm cells from infertile male smokers, although their mitochondrias were not altered. Further research is needed to study the potential negative effects of cigarette on gametes.