Human fertility ability is low in comparison with other animals. The only biological factor of a woman is not responsible for the increasing trend of infertility issue, but research findings reported male factor is also responsible for this issue.
There is a very minimum number of young men (age between 18 years to 25 years) fall under the strict criteria followed under WHO guideline for normal sperm count level. Researchers expected that inherently human becomes vulnerable for a low level of spermatogenesis.
This is a high time to identify the factor responsible for low sperm count along with taken measures for improving sperm production in young adult males to limit the further disruption of human fertility.
After puberty normal healthy male individuals have maintained spermatogenesis throughout the rest of their life. Previously it has proven that during the spermatogenic process of a male individual directly affected by lifestyle factors or exposure to toxic substances from the general environment or due to occupational hazards.
But later it has indicated that disturbances during pregnancy may provide a consequent impact on the quality of spermatogenesis in adulthood, as spermatogenesis is laid during fetal development.
How does masculinization develop in the fetus?
Sertoli cells are the first cells to differentiate and lay down in the process of testis differentiation. It has also anticipated that signals transmitted through Sertoli cells are responsible for organizing the coordination within the testis.
However, the detailed mechanism is not completely understood. The seminiferous cords formation is quite a critical event as they act as originators of seminiferous tubules. The initial phase starts from germ cells, which are surrounded by the Sertoli cells. These germ cells are then transferred into the gonad.
In the subsequent step, peritubular myoid cells are attracted and enclose the Sertoli–germ cell complex to build a seminiferous cord. Along with the Sertoli cells and germ cell proliferation, seminiferous cords have fastened with each other at the terminal ends present in the testis.
At this time, testosterone production from the fetal Leydig cells, which are present in the interstitial spaces between the seminiferous cords. Production of testosterone initiates the masculinization of the fetus.
How maternal lifestyle affects sperm counts or Sertoli cell number in her baby son?
- The testicular dysgenesis syndrome may occur due to impaired production of testosterone and may alter the Sertoli cell proliferation. And if so, then resultant of this leads to low sperm count in the adult age. A research finding reported that maternal high BMI hurts the semen quality in resulting sons at their adulthood, which indirectly indicates maternal obesity has a link with a reduced number of Sertoli cells.
- The increasing trend of environmental chemicals exposure during pregnancy disrupts hormonal activity, specifically androgenic activity. Laboratory-based animal research has proven exposure of chemicals disrupt masculinization and researchers expected the same effect may also occur in humans. Scientific evidence had found a link between chemical exposure at the perinatal stage and low sperm counts in adulthood. Therefore, maternal lifestyle, diet, and chemical exposure are considerable factors in the case of low sperm counts of her son at adulthood.
- Some of the chemicals like organochlorine compounds, polychlorinated biphenyls, pesticides can be accumulated in fat due to their lipophilic nature. Therefore, researchers expected that the scope of such chemical accumulation is higher in obese female and then these chemicals transmitted during pregnancy and lactation to their infants.
- Exhaust fumes, smoke and cooking processes also contain some chemicals like polycyclic aromatic hydrocarbons bind with aryl hydrocarbon (Ah) receptor present in the human body just like dioxin, an environmental chemical. Exposure to such chemicals during pregnancy can reduce sperm production of the male children at their adulthood by reducing the number of Sertoli cells through activating the Ah receptor. The Seveso accident happened in 1976 was the evidence of such incidence. A similar type of adverse effect can occur in case frequent exposure to diesel/car exhaust fumes during pregnancy, as the chemicals affect Ah receptor action.
- Air pollution and maternal smoking badly lower sperm count in the male child at their adulthood due to decrease number of Sertoli cells. Polycyclic aromatic hydrocarbons released during smoking may interact with the Ah receptor. Several large scale studies also supported that men whose mothers had smoked heavily in pregnancy face the challenge of low sperm count.
- Intake of excess amount of saturated fat including meat and administration of anabolic steroids during pregnancy lower sperm counts in the male child at their adulthood.
- Usage of cosmetics, toiletries and/ or medications during pregnancy also increase the risk of maternal exposure to a range of environmental chemicals, which increases the risk of testicular dysgenesis syndrome along with low sperm counts in their male children.
However, it is important to know that maternal exposure to anti-androgenic chemicals during a specific stage of fetal development, which is termed as ‘masculinization programming window’ specifically affects the spermatogenesis by reducing Sertoli cell number in male sons at their adulthood.
Reference: Royal Society Publishing
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