CONICET | Buscador de Institutos y Recursos Humanos

Infertility affects up to 15% of reproductive-aged couples worldwide. Evidence is mounting that lifestyle factors, such as exposure to chemicals and diet, affect uterine functions and maycontribute to infertility. We evaluate the consequences of cafeteria diet and pesticide exposure on uterine development and female fertility. Using a rat model we observed that low doses of endosulfan and low doses of a glyphosate-based herbicide disrupt the expression of genes that regulate uterine development and differentiation during the pre-pubertal period. In addition, we studied long-term effects of pesticides and cafeteria diet onreproductive performance and implantation and post-implantation processes. Both pesticides affected female fertility, but in different ways. Low doses of endosulfan decreased the number of implantation sites. In the case of the glyphosate-based herbicide, there isan increased number of resorption sites. To address the effects of postnatal pesticide exposure on the pregnant uterus, we evaluated the endometrial proliferation and the expression of implantation and decidualization-associated genes. Both pesticides impaired endometrial proliferation and altered the expression of endocrine-regulated gene pathways. The cafeteria diet did not produce subfertility but the foetal growth and placental development were altered. In addition, we found epigenetic modifications associated with the alteration of uterine gene expression. Based on the evidence presented here and previously published data, we conclude that some pesticides and cafeteria diet are likely to diminish fertility in a laboratory animal model. More studies are needed to identify that these lifestyle factors may contribute to the decline in human fertility observed in the past decades.