Role of DNA methylation in bisphenol A exposed mouse spermatocyte.

ABSTRACT

As a widespread environmental contaminant, bisphenol A (2,2-bis(4-hydroxyphenyl)propane, BPA) has been implicated in male reproductive function injury. Previous studies have investigated the mechanisms of DNA damage and oxidative stress caused by BPA; however, little is known regarding its impact on DNA methylation. In this paper, we assessed the adverse effects of BPA on mouse spermatocytes and investigated a potential role of DNA methylation. We demonstrated that BPA exposure inhibited cell proliferation, reduced the DNA replication capacity, and triggered apoptosis in GC-2 cells. In addition, the global DNA methylation levels increased, and the relative expression levels of DNA methyltransferases (DNMTs) varied following BPA exposure. Thousands of distinct methylated sites were screened using microarray analysis. The expressions of myosin-binding protein H (mybph) and protein kinase C δ (prkcd) were verified to be regulated by DNA methylation. These findings indicate that BPA had toxicity in spermatocytes, and DNA methylation may play a vital role in the regulation of BPA-triggered spermatocyte toxicity.