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• Prenatal exposure to EE2 and Pe does not affect ovarian biometric data; • Exposure to EE2 and Pe during the prenatal period cause alters folliculogenesis; • Exposure to Pe reduces the number of follicles and increases the atretic bodies. Exposure to 17α-ethinylestradiol (EE2), a synthetic estrogen, during the developmental period has been found to induce pathological changes in the morphology and function of the gerbil ovary. However, the extract of pequi oil from the fruit Caryocar brasiliense Cambess exhibits anti-inflammatory, antifungal, and anticarcinogenic properties. This study aimed to assess the effects of prenatal exposure to pequi oil and EE2 on ovarian folliculogenesis in gerbils. Pregnant female gerbils were divided into five groups: Control ; EE 2 , which received EE 2 (15 µg/kg/day) during gestation; Vehicle ( Ve ), which received only the vehicle; EE 2 /Pe , which received EE2 and pequi oil (300 mg/kg); and Pe , which received only pequi oil. Female offspring were euthanized at 12 months of age, and their ovaries underwent histological processing. Body and ovarian weights remained unchanged in this study. However, the experimental groups showed a decrease in the number of primordial follicles compared to the control group. Notably, the EE2/Pe group exhibited an increase in the number of secondary follicles compared to the other groups. Statistical analysis revealed significant differences in the number of atretic follicles among the groups, with both the EE 2 /Pe and Pe groups exhibiting the highest numbers of atretic follicles. In summary, the detrimental effects on ovarian morphophysiology induced by EE2 exposure during pregnancy were evidenced by a global reduction in ovarian follicles and an increase in the number of atretic follicles. Consequently, the indiscriminate use of endocrine disruptors, particularly during pregnancy, can lead to significant alterations in the ovarian reserve.
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Silva et al. (2024) studied this question.
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