Prenatal exposure to bisphenol S and bisphenol A differentially affects male reproductive system in the adult offspring.

Early exposure to bisphenol may result in adverse reproductive health in later life. The use of bisphenol S (BPS) has increased considerably after bisphenol A (BPA) is regulated worldwide. However, little is known about the fetal exposure to BPS compared with BPA and its effects on the reproductive system in the adult male offspring. Here, we investigated the effects of orally administered BPS and BPA (0.4, 4.0, 40.0 μg/kg bw/d) during gestation (gD4-21) on testicular development by evaluating the sperm DNA damage & methylation and testicular functions in the 90 d Wistar rats. Male offspring prenatally exposed to BPS (0.4 μg/kg) had higher plasma testosterone than BPA and control. The testis histology reveals thickened membrane by producing a wide interstitial gap between seminiferous tubules, increased testicular inflammation, oxidative stress, TIMP-1 expression, and decreased VCAM-1 expression. BPS promotes apoptosis by up-regulating IL-6, cleaved caspases, and a spike in sperm DNA fragmentation. Prenatal BPS exposure reduces sperm motility mediated via impaired PI3K-AKT signaling and increases testicular TEX11 expression in the offspring. Exposure of the fetus to BPS interferes developmental programming of the male reproductive system in the offspring. BPS could be an equally potent endocrine disruptor affecting male reproductive functions.
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