Abstract

Pregnant mice (n = 3) were exposed to BPA by intraperitoneal injection, from gestation day 9.5 until end of lactation. Male offspring were evaluated for cytokine production at 20 wk-of-age. One pregnant control mouse produced no males, precluding statistical analysis. However, recurring shifts in cytokines were suggested in the adult BPA offspring. Serum showed a numeric increase in 16 of 21 basal cytokine levels. ConA-stimulated splenocytes showed a numeric increase in 17 of 21 cytokines, and LPS-stimulated splenocytes an increase in 18 of 21 cytokines. The cytokine profile was one of TH1 up-regulation more than TH2, and with skewing toward TH17 responses.

Highlights

  • Bisphenol A (BPA) is a monomer component of polycarbonate plastics and epoxy resins used in numerous products of intimate human contact

  • Growing concerns exist over potential adverse effects that may result from BPA exposure during development, due to the transplacental transfer of the chemical [3]

  • 16/21 cytokine levels were numerically greater in the perinatally-exposed BPA mice (Table 1)

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Summary

Introduction

Bisphenol A (BPA) is a monomer component of polycarbonate plastics and epoxy resins used in numerous products of intimate human contact. These include toys, beverage containers, food packaging, medical devices, dental sealants and composites, and plastic pipes carrying household drinking water [1]. Emerging studies show BPA binds estrogen receptor-beta (ERβ), and binds with high affinity to the non-classical membrane-bound ER (ncmER; called estrogen-related receptor-gamma; ERRγ) and a seven-trans-membrane ER designated GPR30 [1]. When the action of BPA is mediated through ncmER or GPR30, its potency can be as high as that of estradiol [6]. The present studies used a cytokine array in serum and the culture supernatants of mitogen-activated splenic lymphocytes in adult mice that had undergone perinatal exposures to BPA, to look for signs of postnatal cytokine skewing as a result of developmental exposure to BPA

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