1Department of Clinical Chemistry, Faculty of Medical Laboratory Sciences, Shendi University, Shendi, Sudan
2Department of Medical Microbiology, Faculty of Medical Laboratory Sciences, Shendi University, Sudan
3Department of Metabolism, Digestion and Reproduction, Imperial College, London W12 0NN, UK
4Obstetrics and Gynecology Department, Faculty of Medicine, ELsheikh Abdallah Elbadri University, Sudan
4Assistant Professor, Microbiology Department, Faculty of Medicine, Elsheikh Abdallah Elbadri University, Sudan
Male fertility depends on spermatogenesis, the intricate process by which sperm cells form in the testes. Current understanding of its physiological mechanisms, endocrine regulation, and susceptibility to environmental and lifestyle variables is summarised in this study. Meiosis (genetic recombination), spermatogonogenesis (mitotic proliferation of spermatogonia), and spermiogenesis (morphological maturation into spermatozoa) are the three main stages of the process. Sertoli cells (nutrition, phagocytosis) and Leydig cells (testosterone production) provide intrinsic support for these processes. Numerous hormonal, genetic, and environmental factors-including temperature-control this process. For proper spermatogenesis development from the earliest stages of spermatogonia proliferation to germ cell maturity, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone (T) are crucial for hormonal regulation. Other hormones, such as activin and inhibin, play a delicate role in regulating the spermatogenesis process. Importantly, this process is severely hampered by lifestyle and environmental factors. By interfering with testicular thermoregulation, scrotal hyperthermia (caused by sedentary employment or laptop use) lowers the number of sperm. Obesity (BMI >25) reduces sperm counts by 25% by increasing oestrogen and decreasing testosterone. Sertoli-germ cell connections are harmed by heavy metals (like cadmium) and occupational pollutants (such as glycol ethers and pesticides like DBCP). Up to 40% fewer sperm are produced by sons of pregnant mothers who smoke. It is concerning to note that 15-20% of young men in Europe have subfertile sperm quantities (<20 million/ml). Environmental endocrine disruptors (such as phthalates) and the combination of chemical exposures and obesity are examples of emerging hazards. The study urges more investigation into the foetal causes of spermatogenic disruption and emphasises the need for immediate public health measures to reduce these hazards.
Keywords: Spermatogenesis; Testosterone; Sertoli Cells; Endocrine Disruptors; Male Infertility; Environmental Toxins
Mosab Nouraldein Mohammed Hamad., et al. “Processes, Regulation, and Environmental Impacts of Spermatogenesis: A Review”. EC Gynaecology 14.10 (2025): 01-16.
© 2025 Mosab Nouraldein Mohammed Hamad., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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