Glyphosate herbicide disrupts the development of the uterus of female rats when they are exposed for 7 days after birth, a recent study (abstract below) by Argentine researchers shows.
The glyphosate herbicide caused cell proliferation and structural changes in the rats’ uterus. This was in spite of the fact that no signs of chronic or acute toxicity or differences in weight gain were seen in treated pups.
Glyphosate herbicide also disrupted the expression of proteins involved in uterine development.
The authors conclude that exposure to glyphosate herbicide may affect female fertility and/or promote the development of uterine cancer.
They also state that their study is the first to show endocrine-disrupting effects of a glyphosate-based herbicide on the uterus of newborn and prepubertal rats, supporting the possibility that glyphosate-based herbicides might be endocrine disruptors.
Neonatal exposure to a glyphosate based herbicide alters the development of the rat uterus
Schimpf, Marlise Guerrero, Milesi, Maria M., Ingaramo, Paola I., Luque, Enrique H., Varayoud, Jorgelina
Toxicology (2016)
http://dx.doi.org/10.1016/j.tox.2016.06.004
Glyphosate-based herbicides (GBHs) are extensively used to control weeds on both cropland and non-cropland areas. No reports are available regarding the effects of GBHs exposure on uterine development. We evaluated if neonatal exposure to a GBH affects uterine morphology, proliferation and expression of proteins that regulate uterine organogenetic differentiation in rats. Female Wistar pups received saline solution (control, C) or a commercial formulation of glyphosate (GBH, 2 mg/kg) by sc injection every 48 h from postnatal day (PND) 1 to PND7. Rats were sacrificed on PND8 (neonatal period) and PND21 (prepubertal period) to evaluate acute and short-term effects, respectively. The uterine morphology was evaluated in hematoxylin and eosin stained sections. The epithelial and stromal immunophenotypes were established by assessing the expression of luminal epithelial protein (cytokeratin 8; CK8), basal epithelial proteins (p63 and pan cytokeratin CK1, 5, 10 and 14); and vimentin by immunohistochemistry (IHC). To investigate changes on proteins that regulate uterine organogenetic differentiation we evaluated the expression of estrogen receptor alpha (ERα), progesterone receptor (PR), Hoxa10 and Wnt7a by IHC. The GBH-exposed uteri showed morphological changes, characterized by an increase in the incidence of luminal epithelial hyperplasia (LEH) and an increase in the stromal and myometrial thickness. The epithelial cells showed a positive immunostaining for CK8, while the stromal cells for vimentin. GBH treatment increased cell proliferation in the luminal and stromal compartment on PND8, without changes on PND21. GBH treatment also altered the expression of proteins involved in uterine organogenetic differentiation. PR and Hoxa10 were deregulated both immediately and two weeks after the exposure. ERα was induced in the stromal compartment on PND8, and was downregulated in the luminal epithelial cells of gyphosate-exposed animals on PND21. GBH treatment also increased the expression of Wnt7a in the stromal and glandular epithelial cells on PND21. Neonatal exposure to GBH disrupts the postnatal uterine development at the neonatal and prepubertal period. All these changes may alter the functional differentiation of the uterus, affecting the female fertility and/or promoting the development of neoplasias.
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