Effects of bisphenol S and bisphenol F on human spermatozoa: An in vitro study.

Bisphenol A (BPA), the main chemical monomer of epoxy resins and polycarbonate plastics, has generated concerns about its endocrine disruptor properties, along with the reported possible links with several human health disorders. Accordingly, some restrictions on its use have been recommended. Bisphenol S (BPS) and bisphenol F (BPF) are the main replacements to BPA, with which they share homologies in chemical structure. However, to date, little is known about their possible adverse effects for human reproduction. As the in vitro exposure of human spermatozoa to BPA induces oxidative/pro-apoptotic effects, the aim of the present study was to verify whether BPS and BPF could represent safer compounds for human sperm functions. The exposure of motile sperm suspensions to scalar concentrations of BPS or BPF for 4 h did not significantly reduce sperm motility (as assessed by computer-aided semen analysis) and viability. At flow cytometry, no changes in mitochondrial membrane potential, or mitochondrial generation of reactive oxygen species were detected by using the JC-1 and MitoSOX red probes, respectively. Interestingly, it nor even the combination of both BPS and BPF at the highest concentrations impaired sperm mitochondrial functions. In conclusion, BPS and BPF seem to be safer alternatives to BPA for sperm biology, as they do not affect mitochondrial functions, sperm motility and viability. These findings could help regulatory agencies to identify more secure chemicals to replace BPA in industrial production of plastics.

In vitro exposure of human spermatozoa to bisphenol A induces pro-oxidative/apoptotic mitochondrial dysfunction.

As bisphenol A (BPA) exerts oxidative/pro-apoptotic effects in several cell types, we explored whether the in vitro exposure to BPA could affect human sperm integrity through the induction of pro-oxidative/apoptotic mitochondrial dysfunction. The exposure of motile sperm suspensions to scalar BPA concentrations for 4h produced a decrease in the mitochondrial membrane potential, starting from 300µM. It was associated with an increased mitochondrial generation of superoxide anion, caspase-9 and caspase-3 activation and motility decrement. Vitality decline was observed at BPA≥400µM. Twenty hours exposure to 300µM BPA, but not to lower concentrations, produced a significant loss in sperm vitality associated with a complete sperm immobilization. Finally, 300µM BPA also produced a significant DNA oxidative damage, as revealed by the formation of oxidized base adduct 8-hydroxy-2'-deoxyguanosine. In conclusion, BPA affected human sperm integrity by inducing pro-oxidative/apoptotic mitochondrial dysfunction.