The influence of nicotine exposure on the male reproductive system
It is well documented that cigarette smoking and nicotine exposure create widespread physiological disorders in humans and animals. The primary tobacco constituent that is responsible for the toxicological consequences associated with the effects of tobacco smoke is nicotine (Van Lancker 1977). After maternal nicotine exposure, the fetal gonads and lungs are the principle sites of nicotine damage (Szuts et al. 1978, Mosier & Jansons 1972). Whilst the fetal lung has received widespread attention in this regard (Maritz 1988), the testis has never been studied. Therefore, I have chosen to explore the effects of maternal nicotine exposure on the testis of male offspring by evaluating various aspects of the male reproductive tract. It is believed that, in adult male smokers (Rosenberg 1987, Handelsman et al. 1984) and sexually mature animals (Mattison 1982) that are exposed to nicotine, male fertility may be compromised. However, these studies provide conflicting data on single parameters. It was therefore my objective to identify the effect of nicotine exposure on the male reproductive tract and to establish possible sites through which these effects may be mediated in adult male rats. The influence of nicotine was then investigated in male offspring after maternal nicotine treatment (MNT), and in sexually mature adult males after direct adult nicotine treatment (ANT). In the former experiment (MNT), 7 day pregnant rats were exposed to Img nicotine/kg body weight/day. Therefore, these offspring were indirectly exposed to nicotine during fetal development and early neonatal development. After weaning the animals were divided into two groups. One group did not receive further treatment (withdrawn group), whilst the other group was continually treated till adulthood (nicotine group), after which both groups were sampled together with the control. In the latter experiment (ANT), the animals were treated daily for 3 weeks and were sampled as above (MNT animals). The fundamental parameter investigated in both experiments to assess reproductive status was sperm quality (motility and morphology). Thereafter, it was necessary to establish a possible site where the effects of nicotine would occur. Testicular growth, epididymal structure, and plasma testosterone content were measured as probable localities of nicotine's effect. The results signify that maternal nicotine exposure poses a greater threat to the male reproductive system than adult nicotine exposure. In the MNT experiment, progressive sperm motility of the nicotine and withdrawn groups were 1.7% and 3.4% respectively. The proportion of abnormal sperm was 72% in each of the above groups. The lower quality sperm that is evident after nicotine exposure implies that the fertilizing ability of the animals may be impaired during adulthood. The data on testicular growth indicates that nicotine exposure during early development results in slower testicular development until maturity. The epididymal lining of these animals also increased after nicotine exposure, indicating increased cellular activity. However, these results from testicular and epididymal studies are inconclusive and need further work. In the ANT experiment, progressive sperm motility of the nicotine group was 1.2%, whilst the proportion of abnormal sperm was 58%. No other parameter was affected after nicotine exposure to adult animals. From the above data it is evident that nicotine exposed animals were subject to greater nicotine damage after maternal nicotine exposure during early development. Moreover, within the maternal nicotine treated experiment, the withdrawal of nicotine after weaning did not appear to reverse the injurious effects of nicotine that were established during early development. These effects were evident since the nicotine and withdrawn groups showed similar levels of damage in all instances. The most profound effects after adult nicotine exposure and maternal nicotine exposure were on sperm quality. The probable site of sperm impairment appears to be via retarded testicular growth and possibly, structural status of the epididymis after maternal nicotine exposure. The results from adult nicotine exposure however, suggest that sperm cells may be directly affected by nicotine exposure. An epidemiological survey was included to validate the basic conclusions established in animal research when compared to clinical data from human patients. No statistically significant changes were observed in this study between the patient's spermiogram results versus his smoking habits, and, that of his mother. From the level of significance it was concluded that cigarette smoking does not appear to be a cause of impaired fertility in already infertile patients. However, the data does suggest that cigarette smoking may well be a precipitating agent in male infertility. Experimentally, nicotine exposure impairs the male reproductive system to some extent. The effects of which are irreversible after indirect exposure (MNT) during development and may begin with poor testicular development. The effects of adult nicotine exposure implies that nicotine exposure in mature animals (ANT) acts directly on sperm cells to incapacitate them. It is well advised that cigarette smoking should be curbed in pregnant women and in adult males to alleviate contributing effects to male infertility.