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. 2012 Sep 24;109(43):17525–17530. doi: 10.1073/pnas.1207854109

Fig. 2.

Fig. 2.

Comparison of meiotic defects in BPA-exposed and placebo-treated fetuses. (AC) Images of pachytene cells. (A) normal, (B) cell with two synaptic defects (arrows), (C) cell with associations involving at least four centromeres. Cells were immunostained with an antibody to SYCP3 to detect the synaptonemal complex (red) and CREST (blue) to visualize centromeres. (D) Frequency of synaptic defects in single daily oral and continuously exposed fetuses. For both exposures, synaptic defects were slightly, although not significantly, increased (χ2 = 0.3, P = 0.9 and χ2 = 3.6, P = 0.17 for single and continuous, respectively) in BPA-exposed fetuses (black bars) compared with placebo controls (gray bars). Values represent mean ± SEM; data represent 118 cells from four females given a single daily oral dose compared with 135 cells from controls, and 105 cells from six continuously exposed females compared with 83 cells from two controls. (E) Comparison of centromere associations in oocytes from BPA-exposed (black bars) and placebo-treated (gray bars) fetuses. Bars represent mean ± SEM. The number of cells with associations was not significantly different between animals receiving single daily oral BPA doses and controls (χ2 = 0.5; P = 0.9) but was significantly increased in fetuses continuously exposed to BPA (χ2 = 11.8; P = 0.01).