This manipulation resulted in four groups of pups, based on their BPA exposure, BPA-BPA: both prenatal and postnatal exposure to BPA, BPA-N: only prenatal exposure, N-BPA: only postnatal and N-N: no BPA exposure.
IgG1 anti-OVA concentrations in sera from these four groups of pups did not differ.
Similarly to what was observed for clinical signs, all groups of pups fed neutralizing VHHs showed significantly lower rates of viral shedding than the control groups.
These transfers created four groups of pups that allowed us to test our hypothesis that the prenatal exposures to BPA were required to promote the development of allergic asthma in our mouse model.
We were able to identify groups of pups that were perinatally exposed to low doses of BPA (0.025 µg/kg bw/day) with robust statistical models (Q2 > 0.4), even at a very early age (PND2).
The first group of pups were examined at three days of age, and the second within 2 hours of birth, so that both groups of animals were at the equivalent age.
Due to the hemolytic property of sodium selenite [31], a significantly (p < 0.05) elevated bilirubin level (twofold increase) was noted in selenite-induced group of pups.
Their pups showed much the same responses to PBBs as did the original group of pups.
Pups from one strain were replaced with a group of pups from the alternate strain within 12 h of birth.
Another group of pups were perfused transcardially with heparinized saline followed by 4% paraformaldehyde in 0.1 M phosphate buffer (pH 7.4).
