Bisphenol-A Affects Male Fertility via Fertility-related Proteins in Spermatozoa

Abstract

The xenoestrogen bisphenol-A (BPA) is a widespread environmental contaminant that has been studied for its impact on male fertility in several species of animals and humans. Growing evidence suggests that xenoestrogens can bind to receptors on spermatozoa and thus alter sperm function. The objective of the study was to investigate the effects of varying concentrations of BPA (0.0001, 0.01, 1, and 100 μM for 6 h) on sperm function, fertilization, embryonic development, and on selected fertility-related proteins in spermatozoa. Our results showed that high concentrations of BPA inhibited sperm motility and motion kinematics by significantly decreasing ATP levels in spermatozoa. High BPA concentrations also increased the phosphorylation of tyrosine residues on sperm proteins involved in protein kinase A-dependent regulation and induced a precocious acrosome reaction, which resulted in poor fertilization and compromised embryonic development. In addition, BPA induced the down-regulation of β-actin and up-regulated peroxiredoxin-5, glutathione peroxidase 4, glyceraldehyde-3-phosphate dehydrogenase, and succinate dehydrogenase. Our results suggest that high concentrations of BPA alter sperm function, fertilization, and embryonic development via regulation and/or phosphorylation of fertility-related proteins in spermatozoa. We conclude that BPA-induced changes in fertility-related protein levels in spermatozoa may be provided a potential cue of BPA-mediated disease conditions.

Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways

“…BPA increases the levels of intracellular peroxides and mitochondrial superoxides and induces apoptotic cell death in neuronal cells by the generation of reactive oxygen species (ROS) and activation of MAPKs and nuclear factor-B (13,14). Accumulated evidence supports the toxic effects of BPA and the resulting pathogenesis of neurodegenerative as well as other diseases (15)(16)(17)(18)(19)(20)(21)(22). BPA exposure resulted in a significant increase of oxidative stress, as evidenced by the increased malondialdehyde levels, decreased glutathione levels, and superoxide dismutase activity in the brain (15)(16)(17)(18)(19)(20)(21).…”

Bisphenol A accelerates capacitation-associated protein tyrosine phosphorylation of rat sperm by activating protein kinase A

“…In mice, male animals exposed to BPA at the level of 25 and 100 ng/kg body weight showed a significant reduction in testicular and epididymal sperm counts [9]. In vitro exposure data on mouse sperms showed that 100 μM BPA resulted in the increase of the capacitation-associated protein tyrosine phosphorylation and the decrease of motility, and induced a precocious acrosome reaction [25]. Figure 4.…”

Clinical utility of sperm DNA fragmentation testing: practice recommendations based on clinical scenarios

“…Rahman et al recently revealed that high concentrations of BPA can alter sperm function, fertilization, and embryonic development via regulation and/or phosphorylation of fertility-related proteins in spermatozoa (96). Bisphenol A was also found to alter sperm DNA integrity.…”