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Table 2 Effects on oocytes of prenatal and postnatal BPA exposure

From: Bisphenol a and the female reproductive tract: an overview of recent laboratory evidence and epidemiological studies

Study Sample Dose Route of administration Time of exposure Results
Zhang et al. [29] Pregnant mice 0.02, 0.04, 0.08 mg/kg bw/day Oral route 12.5-18.5 day post-coital Inhibition of meiotic progression to prophase I in 0.08 BPA treated group; decreased mRNA expression of specific meiotic genes; inhibition of germ cell cyst breakdown
Hunt et al. [30] Pregnant rhesus monkeys 400 μg/kg bw/day tubing implants GD 50–100, GD 100 to term Disturbances in prophase events; increase in MOFs
Susiarjo et al.[31] Pregnant mice, offspring 400 ng/day pellets releasing BPA GD 11.5-17.5 Aberrant meiotic prophase; increased aneuploidy in eggs and embryos from adult females
Rivera et al. [32] Lambs 50 μg/kg/day Subcutaneous injections PND 1-14 Decreased ovarian weight; increased primordial-to-primary follicle transition; increased incidence of MOFs; increased number of small antral atretic follicles associated with higher p27 expression
Karavan et al. [33] Mice 10, 100 μg/day Subcutaneous injections PND 1-4 Increased incidence of MOFs; increased total number oocytes; increased percentage of primordial follicles
Rodriguez et al. [35] Rats 0.05, 20 mg/Kg/day Subcutaneous injections PND 1-7 In BPA 20 group stimulation of neonatal initial follicle recruitment; p27 and ERα increased expression; increased proliferation rate of granulosa cells
Chao et al. [36] Mice 20, 40 μg/kg Subcutaneous injections PND 7–14, PND 5–20 (every 5 days) Decreased methylation pattern of two maternal imprinted genes; upregulated mRNA expression of ERα; decreased primordial follicle number but increased primary, secondary and antral follicle number; abnormal spindle assembling in meiosis