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Table 5 Effects of pesticides on ovarian function

From: Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data

References Methods Results
Animal Data
Zama and Uzumcu, 2009 [57] Prenatal exposure of pregnant rats to MXC 20 μg or 100 mg/kg/day from embryonic D19 until postnatal day 7. DNA hypermethylation of several ovarian genes among which ER beta.
DNA methyltransferase 3b (DNMT3b) levels in ovaries at 100 mg/kg/day
Park et al., 2014 [53] Oral exposure of pregnant mice from gestational D12 to post-natal day 20 with 5 to 500 μg/kg dose of Simazine. Ovarian weight and apoptosis of granulosa cells in the F1 generation with downregulation of anti-apoptotic and proliferation genes
El-Sharkawy et al., 2014 [54] Oral exposure of female rats to 200 mg/kg twice weekly to MXC alone, or combined with propolis (a natural anti-oxydant) 200 mg/L for 10 months Ovarian weight, atresia of primary, secondary and antral follicles, ovarian antioxidant status and in ovarian lipid peroxidation. Toxic effect neutralized using Propolis
Satar et al., 2015 [52] Oral exposure of adult female rats to methyl parathion, every day for 8 days. Followed by ovarian histological analysis Structural alteration of the ovarian stroma with apoptosis phenomena in follicles during chronic exposure. = Alteration of follicular capital
Kotil and Yön, 2015 [51] Oral exposure of adult rats to permethrine, 20 or 40 mg/kg/day for 14 days. Ovarian histological evaluation Picnotic nucleus, condensed chromatin, alteration to the mitochondrial structure
Human Data
Farr et al., 2006 [58] Epidemiological study on 8038 women who live and work in rural American median age at menopause by 3 months (OR = 0.87, CI 95% = 0.78–0.97) and at 5 months (OR = 0.77, CI 95% = 0.65–0.92) depending on the type of pesticides used