Sperm Traits and Male Fertility in Natural Populations
Written by Ben Bunting: BA(Hons), PGCert.
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While the majority of studies on sperm traits and male fertility in human populations have used men from infertility clinics, the results of such studies are not necessarily representative of the general population. Population-based studies, for example, have demonstrated regional and ethnic differences in semen analyses. This means that male fertility can vary significantly depending on the environment and the genes present in the semen.
mtDNA is a factor involved in spermatogenesis
The sperm development process is divided into distinct stages. Each stage is represented by a different type of sperm cell. For example, Type A spermatogonia produce pairs of interconnected cells. Type A-paired spermatocytes form chains of four to sixteen cells.
The role of mitochondria in spermatogenesis is widely studied. Mutations in mitochondrial DNA can lead to altered sperm motility. Several haplogroups have been linked to reduced sperm motility. Specifically, the mtDNA haplogroup R was found to have an effect on sperm motility.
Sperm mitochondria contain mtDNA that is passed down from the mother to her offspring. This mtDNA is inherited via interspecific mouse crosses, but paternal mtDNA is excised from the fertilized egg cell during a subsequent backcross. The mtDNA copy number in the paternal gamete is much smaller than in the egg. Also, sperm contain about 100 copies of mtDNA, which is much less than what is found in an egg.
Mitochondrial dynamics drive spermatogenesis in multiple species, including mice and Drosophila. In Drosophila, Dmfn, Opa1, and Drp1 are required for the post-meiotic stage of spermatogenesis. These findings suggest a role for mitochondrial dynamics in human spermatogenesis and may lead to the development of novel contraceptives.
In spermatogonia, mitochondria are small, but elongate after crossing the BTB. They cluster around the nuage and intermitochondrial cement and are dispersed in post-meiotic spermatids. They are also fragmented in post-meiotic spermatogonium.
Environmental pollution affects spermatogenesis
Recent research has shown that air pollution affects male fertility and sperm quality. It also alters sperm motility, DNA fragmentation, and morphology. In a systematic meta-analysis, researchers found a significant correlation between air pollution and male fertility and sperm quality. Air pollution also affects the levels of reproductive hormones.
Air pollution affects spermatogenesis in animals and humans through the inhalation of gases or solid particles. Air pollutants are either natural or man-made and come from various sources. Among the pollutants present in air are PM2.5 particles and polycyclic aromatic hydrocarbons. These substances are endocrine disruptors that affect spermatogenesis.
In humans, non-essential heavy metals such as Cadmium and Barium can negatively impact male fertility by affecting sperm and semen quality. Studies have shown that exposure to these chemicals results in reduced sperm concentration and abnormal sperm. In addition, heavy metals cause the production of reactive oxygen species (ROS), which can damage sperm DNA and cause infertility. In addition, cadmium and lead are known reproductive toxicants and suspected endocrine disruptors. These substances have long-term effects on male fertility.
In addition, air pollutants such as ozone may affect spermatogenesis. Research has shown that high levels of ozone may reduce the percentage of sperm with normal morphology. This can help explain the rising rates of male infertility. Another key indicator of air pollution is particulate matter 2.5 (PM2.5). Exposure to PM2.5 causes abnormal sperm morphology in males exposed to air pollution.
Testicular temperature influences sperm motility
The study of testicular temperature and sperm motility in natural populations suggests that elevated temperature can impair fertility, alter sperm parameters, and damage membrane integrity. In a recent study, 10 healthy men were exposed to microwave radiation for 30 minutes every three weeks, resulting in intratesticular temperatures between 40 and 42 degrees C (104-108 degrees F). A similar study, based on insulated jockstraps, exposed 14 healthy men to a two-degree increase in body temperature. This led to a decline in total sperm count after three weeks of use.
However, a variety of physical activities have been shown to improve sperm parameters. High-intensity intermittent training has been found to improve oxidant/antioxidant markers in seminal plasma more than moderate-intensity continuous training. In addition, continuous bicycling has a negative correlation with sperm concentration and count.
Among males with testicular temperature-induced infertility, those with higher BMI (body mass index) had lower sperm motility. This may be attributed to higher levels of fatty tissue in the scrotum, which can prevent sperm from cooling properly. Other factors that contribute to higher testicular temperature include varicocele, a condition where the scrotum has numerous varicose veins. Varicose veins are associated with a high prevalence of male infertility and are believed to reduce male fertility.
The relationship between age and sperm parameters has been controversial. The World Health Organization identified the SARS-CoV-2 virus as a pandemic in March 2020. It is spread by saliva droplets, nasal discharges, coughing, and sneezing. This virus can also infect the testes and impair sperm motility.
Roundup herbicide causes Sertoli cell death
This herbicide is linked to Sertoli cell death in males, a condition that impacts male fertility. This condition is caused by a buildup of reactive oxygen species (ROS), which are generated during oxidative stress. These free radicals are implicated in nearly every chronic disease, including cancer, and they play an important role in many processes relating to reproductive health. ROS attack the sperm nucleus and plasma membrane, causing damage to the cell. Over time, they induce DNA damage, accelerate germ cell death, and reduce sperm counts.
In humans, exposure to Roundup causes a decline in sperm count and is associated with increased risk of testicular cancer and male reproductive tract abnormalities. It is also linked with a drop in serum testosterone levels. This suggests that the herbicide is a contributor to the decline in male fertility in natural populations. In addition, Roundup increases the levels of TBARS and protein carbonyls, which are markers of oxidative damage.
It has also been shown that the herbicide Roundup causes Sertoli cell death in male fertility. Similarly, the herbicide DDT causes oxidative stress and may impair mitochondrial function. These legacy pesticides remain in the environment for many years after they were first used. Moreover, the effects of Roundup herbicide on male fertility can be felt for decades to come.
Copper overload impairs sperm motility
Copper deficiency negatively affects male fertility, possibly due to metabolic diseases and genetic preconditions. Several studies have linked Cu to lower sperm motility, decreased sperm concentration, and morphological abnormalities in spermatozoa. A large study on experimental Cu deficiency in rams found that sperm motility and concentration were decreased in Cu-deficient rams.
Iron deficiency also affects male fertility. Anemia inhibits spermatogenesis and causes a hypoxic environment in the testes. Spermatogenesis requires substantial oxygen, and anemic males display low sperm counts and poor sperm parameters. Oxygen diffusion in the testicle is also slow. Anemic males are more likely to have low sperm counts. However, iron supplementation can significantly improve sperm motility.
Copper and iron metabolisms have been linked for decades. An enzyme called ceruloplasmin serves as a fundamental bridge between Fe utilization and Cu status. Ceruloplasmin oxidizes the ferrous ion to ferric, enabling it to be transported with transferrin, which only carries trivalent iron. Almost 50 years ago, Orlando and colleagues confirmed the presence of ceruloplasmin in human testes. Further, they suggested that ceruloplasmin may serve as a marker of seminiferous tubule function.
A new study suggests that a higher intake of antioxidant vitamins and minerals increases sperm quality in older men. While conventional medical treatments have not reversed this global decline, there is evidence to suggest that micronutrient supplementation may help men become more fertile.
Conclusion
Sperm traits are highly heritable, and they are positively correlated with male attractiveness. Unlike male attractiveness, however, sperm viability is not affected by inbreeding depression. In this study, we analyzed the genetic variation in sperm viability in a panel of D. simulans genotypes, pairing genotypes with high and low sperm viability. We then compared the fitness of females with different genotypes in order to assess their fertility.
Sperm traits are related to male fertility in a complicated process called spermatogenesis. It requires a minimum of six weeks to complete and involves a coordinated series of mitotic and meiotic divisions, intricate cyto-differentiative steps, and constantly changing intercellular interactions. A variety of endocrine, paracrine, and autocrine factors control this process.
Although sperm traits are correlated with fertility, studies of natural populations have not yet identified any causal relationships between these traits and male fertility. For instance, there are few studies of natural sperm traits in domestic animals, and their analysis relies on only a few traits. In human populations, however, the development of treatments depends on our ability to understand how these traits impact fertility.
In contrast, pesticide exposure is another factor that can have dramatic effects on spermatogenesis. In one study, workers exposed to the pesticide DBCP had lower sperm counts. Despite this, dietary intake did not affect the semen parameters in these men.
