INVESTIGADORES
VARAYOUD Jorgelina Guadalupe
congresos y reuniones científicas
Título:
Perinatal exposure to glyphosate or Its commercial formulations: uterine molecular mechanisms involved in embryo implantation failures
Autor/es:
PACINI G; LORENZ V; VARAYOUD J; LUQUE EH; MILESI MM
Reunión:
Congreso; Reunión conjunta de sociedades de Biociencias; 2017
Resumen:
Glyphosate-Based Herbicides (GBHs) have been the most widelyused herbicides during the past three decades. Commercial formulationsinclude other chemical, collectively named as co-adjuvants.Although these substances are classified as inert compounds, it hasbeen demonstrated that the formulations of glyphosate are moretoxic than the active principle (glyphosate). In the present study, weinvestigate the effects of perinatal exposure to glyphosate (Gly) ora commercial formulation on female fertility and fetal development.Pregnant rats (F0) were orally exposed to Gly or to a GBH throughfood, in a dose of 2 mg of glyphosate/kg/day (RfD, EPA), from gestationalday (GD) 9 until weaning (lactational day 21). The body weightgain and the vaginal canal-opening of the F1 females were determined.Sexually mature F1 females were submitted to a fertility testto evaluate the pregnancy rates, and on GD19, the number of corporalutea (CLs) and the implantation and resorption sites. To analyzetransgenerational effects on the F2 offspring development, weevaluated the fetal weight, length and morphology, and the placentalweight. Gly and GBH exposure neither altered the body weight gainof the F1 females with age, nor induced changes in vaginal opening.Although all Gly- and GBH-treated F1 females resulted pregnant,a decreased number of implantation sites was detected. Moreover,F2 offspring exhibited a delayed growth, evidenced by lower fetalweight and length in both Gly and GBH groups. No differences inplacental weight were detected but an increase in placental indexwas observed in the Gly group. We concluded that perinatal exposureto Gly or its commercial formulation induced female subfertilityin rats by decreasing the number of implantation sites. In addition,the normal development of their progeny was affected. These resultssuggested that the active principle, Gly, produced these deleteriousreproductive effects.