Endocrine Disruptors As Promoters of Biosphere Carcinogenic Background

The main aim of the study is to analyze modern knowledge on endocrine disruptors, non-genotoxic carcinogens, contributing significantly to the total level of contamination of the biosphere by anthropogenic blastomogens. Material and Methods . For the review preparation, we analyzed articles on molecular mechanisms of the effects of endocrine disruptors, available at biomedical literature databases sciVerse scopus, pubmed, Web of science, Rsci. The review cited 65 recent publications, 21 of them being published over the past three years, 3 papers being the official documents on hazards associated with the use of endocrine disruptors, and 10 papers presenting a background to separate endocrine disruptors into the group of compounds with specific functional activity. Results. The role of endocrine disruptors involves the development of the tumors of reproductive organs. They may reveal the properties of strong agonists or antagonists disrupting the hormonal balance by inhibition of the synthesis of natural hormones, their secretion, transport, metabolism, binding or degradation. In addition, they activate alternative proliferation signaling pathways by activating g-proteincoupled receptors, estrogen-bound eRRγ or/and β-adrenergic receptors. The main mechanism of action of endocrine disruptors is the induction of epigenetic modifications, in particular, methylation/demethylation of cpg dNa islands, histone modifications and changes in expression of non-coding RNa. since the effects of endocrine disruptors are nonlinear, they can be caused by concentrations corresponding to the real content in the biosphere and detected in the umbilical blood and breast milk. In addition, they contribute to the metabolic activation of the procarcinogens, the main component of air pollution, by activation of the cytochrome p450 isoforms. Conclusion . Endocrine disruptors can underlie the development of tumors of hormone-dependent organs both at direct and transplacental exposure.