Perinatal exposure to a glyphosate based herbicide causes implantation failures and transgenerational induction of congenital anomalies in rats

PACINI G; LUQUE EH; ALARCÓN R; VARAYOUD J; MILESI MM

Congreso; LXI Reunión Anual de la Sociedad Argentina de Investigación Clínica, LXIV Reunión de la Sociedad Argentina de Inmunología y XLVIII Reunión de la Sociedad Argentina de Farmacología Experimental; 2016

Sociedad Argentina de Investigación Clínica, Sociedad Argentina de Inmunología y Sociedad Argentina de Fisiología Experimental

Glyphosate based herbicides (GBH) are extensively used for agricultural purposes all over the world, which is closely associated with a constant increase in the use of transgenic glyphosate-resistant soybean single-cropping. Recently, we showed that a brief exposure to a GBH, administered subcutaneously during the first postnatal week alters uterine development in prepubertal rats, and induces post-implantation embryo loss at adulthood. In the present study we evaluate if an oral administration of GBH during the perinatal period (gestation and lactation) affects female fertility and/or induces transgenerational effects on prenatal development of their progeny. Pregnant rats (F0) were orally exposed to 200 mg GBH/Kg/day through food, from gestational day (GD) 9 until weaning (postnatal day 21, PND21). The body weight gain and the vaginal canal-opening of the F1 females were evaluated. On PND90, F1 females were submitted to a fertility test to evaluate the pregnancy rates, and on GD19, the number of corpora lutea (CLs) and the implantation and resorption sites. To determine transgenerational effects on the F2 offspring development, we evaluate the fetal weight, length and morphology, and the placental weight. GBH exposure did not alter the body weight gain of the F1 females with age, but led to early onset of vaginal opening, indicating early puberty. Although all GBH-treated F1 females resulted pregnant, a decreased number of implanted embryos were detected. Moreover, F2 offspring exhibited a delayed growth, evidenced by lower fetal weight and length. A higher placental weight was detected in the GBH group. Surprisingly, structural congenital anomalies, such as, conjoined fetuses and abnormally developed limbs were detected in the F2 offspring. We concluded that perinatal exposure to a GBH induced female subfertility by decreasing the number of implanted embryos, and caused transgenerational induction of congenital anomalies.