EFFECT OF BISPHENOL A ON MALE FERTILITY
DOI:
https://doi.org/10.11603/1811-2471.2023.v.i4.14314Keywords:
bisphenol A, endocrine disruptors, spermatogenesis, male reproductive system, testosteroneAbstract
SUMMARY. A significant proportion of male infertility cases are caused by toxic exposure to chemicals that directly affect human health through the environment. These include endocrine disruptors, a special place among which is occupied by bisphenol A (BPA) – a chemical that has a selective negative effect on the endocrine system. According to many researchers, BPA can cause endocrine dysfunction and negatively affect the male reproductive system.
The aim – to reveal the mechanisms of the effect of bisphenol A on spermatogenesis and the possibility of reproductive ability. Based on the analysis of data from the scientific literature, where experimental animal models were used.
Material and Methods. Analysis and generalization of scientific research publications in the context of the toxic effect of endocrine disruptors on the mechanisms of male fertility are held.
Results. Bisphenol A qualifies as a xenoestrogen because it affects the body like estrogen due to its characteristic polycyclic phenolic structure similar to estradiol. BPA can affect the male reproductive system through the hypothalamic-pituitary-gonadal axis, leading to pathological consequences. It has been suggested that BPA has both short-and long-term effects on men due to changes in their phenotype. It was found that through functional modification of genes, the compound is involved in the differentiation of spermatogenic epithelial cells. In experimental models, exposure to BPA usually led to a decrease in the number of spermatozoa, their motility, normal morphology of spermatozoa was disrupted, their DNA was damaged, and spermatogenesis dysfunction was observed in general, while the negative effect of BPA was observed in a wide range of doses of the drug. At the same time, a number of researchers believe that bisphenol A does not have a destructive effect on the fertility of laboratory rats exposed to the drug in adulthood at low doses, but high doses of BPA negatively affect the fertility of experimental animals.
Conclusions. BPA probably has a negative effect on the male reproductive system through the hypothalamic-pituitary-gonadal axis, reducing fertility. The effect of BPA probably leads to a deterioration in the main parameters of spermatogenesis. In this context, it is important to investigate the complex mechanisms of BPA action on the male reproductive system in order to predict medical consequences and reduce the negative effects of endocrine disruptor on male fertility in order to maintain public health.
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