Background The main objective of this review was to state a hypothetical mechanism of the antitoxic effect of lactoferrin (Lf) on embryos exposed to bisphenol A (BPA). On this basis, it is possible to suggest Lf as a potential protective health component before conception upon toxic effects and viral infections. Methods The narrative review was performed using systematic review methods to identify relevant literature. The resources required for this study were obtained by searching the electronic database PubMed (MEDLINE). Articles were searched using the keywords “BPA,” “lactoferrin,” “DNA‐methylation,” “epigenetic,” “mammals,” “human,” and “mouse.” The inclusion criteria were as follows: (a) primary or original research; (b) study of epigenetic modification; and (c) study focuses on early mammalian development. Results Presented data demonstrate that Lf can modulate epigenetical characteristic, such as DNA methylation and reactive oxygen species (ROS), and, thereby, may serve as a potential readily available pharmaceutical product. Conclusion Suggested hypothesis is based on the important interrelated role of changes in epigenetic modifications and oxidative stress in early embryogenesis under the influence of BPA and virus infection as a cause of the development of pathologies in the adult organism.

BACKGROUND: Bisphenol A is a chemical agent ubiquitous in plastic consumer products and a toxin capable of disrupting key epigenetic mechanisms in early embryogenesis. It becomes more and more clear that early development changes in epigenetic pathways caused by exposure to toxic substances are associated with various adult diseases. Therefore the need to identify new agents capable of eliminating epigenetic mechanisms failures caused by the bisphenol A toxin becomes evident. Here we suggest lactoferrin as a normalizer of toxicant-induced epigenomic changes. Currently there is no data on the role of lactoferrin as a normalizer of epigenomic disorders under the influence of toxicants. We assume that in mammalian embryogenesis lactoferrin might function as an epigenetic modulating factor. AIM: The aim of the research is to study effects of lactoferrin on the epigenetic status of postimplantation mouse embryos, exposed to bisphenol A in utero. MATERIALS AND METHODS: In this study, 3 experimental groups of mice and two control group were used. 1. Mice on the first day of pregnancy, injected with 40 mg/kg of body weight of bisphenol A; 2. Mice on the first day of pregnancy, injected with 50 mg/kg of body weight of lactoferrin; 3. Mice on the first day of pregnancy, successively injected with 50 mg/kg body weight of lactoferrin and 40 mg/kg of body weight of bisphenol A. On the 15th day of embryonic development, the level of genome-wide DNA methylation was evaluated in different body parts of the embryos by methyl-sensitive restriction and ImageJ visualization analysis. RESULTS: We demonstrated that in post-implantation mouse embryos, exposure to bisphenol A in the prenatal period caused an increased level of genome-wide DNA methylation. The most prominent effects were observed in brain and abdominal section of the embryos. Together, the present findings confirmed that lactoferrin administration at a dose of 50 mg/kg of body weight resulted in normalization of genome-wide DNA methylation levels after bisphenol A-induced epigenetic alterations. CONCLUSIONS: We assume that lactoferrin may partially neutralize the harmful effects of bisphenol A caused aberrant methylation, and thus can potentially be used as a pharmaceutical product. Factual findings of the present study may help by development of new therapeutic approaches. Nevertheless, further research of the bisphenol A, lactoferrin and lactoferrin + bisphenol A effects on reactive oxygen species and/or antioxidant enzymes is needed.