Bisfenol A e seus impactos tóxicos na reprodução

Abstract

Bisphenol A (BPA), widely used in plastics and epoxy resins, is a concern due to its ability to interfere with reproductive physiology, embryonic development, and molecular mechanisms associated with its toxicity as an endocrine disruptor. This integrative literature review systematizes in vivo and in vitro experimental evidence on embryotoxicity, gonadal effects, molecular pathways, and transgenerationality associated with BPA exposure. The results indicate that exposure to the compound compromises embryonic development from the early stages, reducing cleavage rates and blastocyst formation, as well as increasing apoptosis and oxidative stress. Mitochondrial dysfunction and metabolic alterations that directly affect embryonic competence are also observed. Regarding gonadal effects, there is a reduction in oocyte quality, alterations in meiotic maturation, spindle disorganization, follicular atresia, and ovarian steroidogenesis dysfunction. At the molecular level, BPA acts primarily by binding to estrogen receptors, inducing reactive oxygen species, modulating apoptotic pathways, and causing epigenetic alterations. Further evidence points to transgenerational effects, with reproductive impacts observed in generations not directly exposed, suggesting persistent epigenetic reprogramming. This experimental article uses an in vitro bovine oocyte maturation model to investigate the effects of different concentrations of BPA on meiotic progression, cellular homeostasis, and subsequent embryonic development. The findings demonstrate that elevated concentrations of BPA during oocyte maturation impair developmental competence, compromising mitochondrial function, increasing intracellular levels of reactive oxygen species, and altering cytoskeletal organization and chromosome alignment. These alterations result in a higher incidence of aneuploidy, reduced embryonic viability, and lower post-fertilization developmental efficiency. Studies show that BPA exerts multifactorial reproductive toxicity, involving endocrine disruption, oxidative stress, mitochondrial dysfunction, epigenetic alterations, and impairments in oocyte maturation and embryonic development. Furthermore, they reinforce that even exposure to BPA can trigger significant and lasting biological effects. Thus, these findings contribute to advancing the understanding of the mechanism of BPA toxicity and highlight its relevance as an environmental risk factor for fertility, embryonic competence, and reproductive health across generations.