In vitroeffects of nicotine on human spermatozoa

Abstract

Washed human spermatozoa from 12 normozoospermic donors were treated with different concentrations of nicotine 0.1, 1.0, 5.0 and 10.0 mm and were compared to spermatozoa suspended in nutrient medium only (control). Computer-aided sperm analysis was used to assess sperm kinematic properties after 30, 60, 120 and 180 min of incubation. Viability was assessed by means of a dye exclusion staining technique (eosin/nigrosin), while acrosome-reacted cells were identified under a fluorescent microscope using fluorescein isothiocyanate-Pisum sativum agglutinin as a probe. Nicotine significantly reduced total motility, progressive motility, curvilinear velocity, amplitude of lateral head displacement, beat cross-frequency, viability and caused spontaneous acrosome reaction at concentrations of ≥5.0 mm after 2 and 3 h of exposure. Nicotine concentrations of 0.1 and 1.0 mm had no significant effect (P < 0.05) on spermatozoa except that 1.0 mm significantly decreased (P < 0.05) sperm progressive motility at 2 and 3 h of incubation as well as viability after 3 h of incubation. This study concludes that the occurrence of high levels of nicotine in the body and seminal fluid might adversely affect fertilisation capacity of human spermatozoa through a mechanism that involves decreased motility, viability and premature induction of the acrosome reaction.

Late reproductive analysis in rat male offspring exposed to nicotine during pregnancy and lactation

“…was the decrease in motility parameters (Reddy et al, 1995;Condorelli et al, 2013;Oyeyipo et al, 2014). However, increase in the occurrence of late apoptotic spermatozoa with altered chromatin compactness or DNA fragmentation (Condorelli et al, 2013), reduced sperm viability (Condorelli et al, 2013;Oyeyipo et al, 2014), and premature induction of the acrosome reaction (Oyeyipo et al, 2014) have also been described in this type of experiment.…”

“…However, increase in the occurrence of late apoptotic spermatozoa with altered chromatin compactness or DNA fragmentation (Condorelli et al, 2013), reduced sperm viability (Condorelli et al, 2013;Oyeyipo et al, 2014), and premature induction of the acrosome reaction (Oyeyipo et al, 2014) have also been described in this type of experiment. Toxicants (such as nicotine) may directly or indirectly target the DNA through oxidative stress (OS) and DNA strand breaks, which are observed in mature spermatozoa; this might injure mitotic spermatogonia or meiotic germ cells, as well as post-meiotic spermatids undergoing spermiogenesis (reviewed by Delb es et al, 2010).…”

Clinical utility of sperm DNA fragmentation testing: practice recommendations based on clinical scenarios

“…Moreover, significant negative correlations were noticed between the degree of DNA damage and worsening of semen parameters (90). Chemicals such as nicotine (125), cadmium (126), lead (127) and benzopyrene (128) were specifically investigated and found to cause sperm DNA damage.…”

Nicotine elevates sperm motility and inducesPfn1promoter hypomethylation in mouse testis

“…In vitro studies have found that neither nicotine nor its metabolite cotinine in low concentrations was harmful to sperm motility (Gandini et al ., ). However, higher nicotine levels (≥1 m m ) significantly decreased sperm motion parameters and viability characteristics (Oyeyipo et al ., ). At higher concentrations, nicotine reduced the percentage of viable spermatozoa and promoted spermatozoa apoptosis, which was accompanied by DNA fragmentation or altered chromatin density.…”