Objectives: Dental resin monomer is suspect of being the environmental estrogens. In the present study we have examined the effects of the prenatal exposure to the dental resin monomers, 2,2-bis(4-hydroxyphenyl)-propane (bisphenolA, BPA), 2,2-bis[4´-(2´-hydroxy-3´-methacryloyoxy) phenyl]propane (Bis-GMA), triethyleneglycoldimethacrylate (TEGDMA) and urethane dimethacrylate (UDMA) on testosterone (T) and estradiol-17b (E₂) levels in serum and T metabolism in testis. Methods: Eighteen pregnant Wistar rats were daily injected subcutaneously with BPA (5µg/day, n=4), Bis-GMA (5µg/day, n=4), TEGDMA (5µg/day, n=2) and UDMA (5µg/day, n=2) on days 12 through 19 of gestation, respectively. Rats treated with vehicle(n=2), corn oil, were used as controls, and diethylstilbestrol (DES, 5µg/day, n=2) or E₂ (5µg/day, n=2) treated rats were used as positive controls. Male offspring were sacrificed at 13 weeks of age and assayed T and E₂ levels in serum. For the in vitro study, after C¹⁴-progesterone (P₄) and testicular homogenate were incubated, the activities of the enzymes related to the T production from P₄ were analysed. Results: DES treated rats were all stillbirth. BPA and E₂ decreased the T in serum and BPA, Bis-GMA, and TEGDMA increased E₂. While, UDMA did not affected the T and E₂ levels in serum. T synthesizing enzymes, 17 a -hydroxylase, C_17-20lyase and 17 b -hydroxysteroid dehydrogenase showed significant increase by the exposure of TEDMA, E₂, Bis-GMA and BPA, in the offspring testis. The data were analyzed by wilcoxon t-test. Conclusions: These results demonstrated that the prenatal exposure to BPA, Bis-GMA and TEGDMA caused the testicular dysfunction and these chemicals had a character of environmental estrogen.

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