The purpose of the review of foreign literature was to analyze current research on the effects of cadmium on male reproductive function. Results. According to the researcher data, at least 15–20% of cases of fertility decline in males fall on infertility. The etiology of this phenomenon in 50% of cases remains unknown, however, increasing environmental pollution contributes to a constant increase in male infertility. One of the most toxic pollutants is cadmium. Numerous animal model studies and human epidemiological studies indicate an adverse effect of cadmium on male fertility. Smoking is an important source of cadmium, which is absorbed into the human body. In vitro studies confirm the deleterious effects of cigarette smoke compounds on sperm motility and spermatozoon parameters. Depending on the concentration, nicotine suppresses the progressive motility of the spermatozoon parameters, starting from the lowest concentration used (1 ng/ml). Likewise, it decreases the percentage of viable spermatozoon parameters and increases the amount of spermatozoon parameters in late apoptosis with altered chromatin compactness or DNA fragmentation already after 3 hours of incubation. On average, the daily intake of cadmium in humans is 1.06 μg/kg body weight, the half-life of cadmium is more than 20-40 years, which causes its accumulation in the body. The testicles are the organ in which cadmium is stored in large quantities. Studies have shown that the testicles are extremely sensitive to cadmium because these organs are characterized by intense cellular activity, where vital spermatogenesis processes take place. Exposure to cadmium leads to reproductive tract abnormalities such as cryptorchidism and hypospadias, testicular cancer, subfertility or infertility, called testicular dysgenesis syndrome. In the genesis of the testicles during the embryonic and neonatal periods, Sertoli’s cells play a critical role, the development of which is influenced by cadmium. Exposure to cadmium (1-2 mg/kg, subcutaneously) in pregnant and lactating rats causes vacuolization of Sertoli’s cells and loss of cells in the epithelium of the seminiferous tubules in adult animals. Cadmium inhibits proliferation, induces apoptosis and DNA damage in immature Sertoli’s cells. Perinatal exposure to cadmium affects the development and function of fetal Leydig cells, which are endocrine cells in the testicle. In pregnant rats that received a single dose of cadmium (0.25, 0.5, and 1.0 mg/kg, intraperitoneally), synthesis of testosterone in the fetal tests was significantly reduced, while gene expression in cells was suppressed, and the androgen-dependent formation process was reduced. The mechanism by which cadmium mediates impaired male fertility is also associated with the production of reactive oxygen species in the testicles, which leads to oxidative stress that interferes with the development and functioning of the spermatozoon parameters. Exposure to cadmium, for both environmental and occupational reasons, can contribute to a decrease in the quality of human sperm, which confirms high toxicity of cadmium. Conclusion. Thus, in humans and other mammals, cadmium damages the male reproductive system, disrupts its structure, including the vascular system of the testicles, leads to DNA damage, inhibits functions of germ cells, leads to loss of sperm quality and quantity, sub-fertility or infertility
Circular RNAs from BOULE play conserved roles in protection against stress-induced fertility decline