Abstract
AimExposure of boar sperm cells to Bisphenol A diglycidyl ether (BADGE) has been shown to lead to reproductive failure in sows, however, the mode of action is unknown. As we have recently shown that BADGE can interfere with Ca2 + signaling in human sperm cells through an action on CatSper, and as CatSper has been shown to be expressed in boar sperm cells, we hypothesized that a similar mechanism in the boar sperm cells could be responsible for the reproductive failure.MethodsDirect effects of BADGE and the endogenous ligand of human CatSper, progesterone, on Ca2+ signaling in human and boar sperm cells were evaluated side-by-side using a Ca2+ fluorimetric assay measuring changes in intracellular Ca2+. Effects of BADGE on Ca2+ signaling in boar sperm were furthermore assessed by flow cytometry by an independent laboratory.ResultsThe exact same solutions of BADGE and progesterone induced transient biphasic Ca2+ signals in human sperm cells, but failed to do so in both non-capacitated and capacitated boar sperm cells. BADGE also failed to induce transient biphasic Ca2+ signals in boar sperm cells in the flow cytometric assay.ConclusionBADGE and progesterone failed to induce Ca2+ signals in boar sperm cells. This indicates that the signaling mechanisms leading to activation of CatSper differs between human and boar sperm cells, and suggests that the mode of action by which exposure of boar sperm cells to BADGE can lead to reproductive failure in sows does not involve effects on Ca2+ signaling.
Highlights
The CatSper Ca2+ channel is a sperm specific Ca2+ channel highly conserved in mammals (Cai and Clapham, 2008), and present in a wide range of other species (Romero and Nishigaki, 2019)
Our results showed that addition of the exact same solutions of Bisphenol A diglycidyl ether (BADGE) and progesterone to the sperm cells, induced transient biphasic Ca2+ signals in the human sperm cells, but failed to do so both in non-capacitated and capacitated boar sperm cells (n ≥ 3) (Figures 1A–C), whereas addition of 10 μM ionomycin induced rapid and saturating Ca2+ signals in both human and boar sperm cells
When comparing the amplitude of the induced Ca2+ signals 30 s after addition of compounds, a time point where both the progesterone- and BADGE-induced Ca2+ signals peak in human sperm cells, we found that BADGE at concentrations ≥3,125 μM induced Ca2+ signals significantly larger than those induced by HTF buffer alone in human sperm cells (Figure 1D). 5 μM progesterone and 10 μM ionomycin, induced significantly larger Ca2+ signals in human sperm cells (Figure 1D)
Summary
The CatSper Ca2+ channel is a sperm specific Ca2+ channel highly conserved in mammals (Cai and Clapham, 2008), and present in a wide range of other species (Romero and Nishigaki, 2019). In human (Lishko et al, 2011; Strünker et al, 2011) and macaque sperm cells (Sumigama et al, 2015) CatSper has been shown to be activated by the female. Boar Sperm Ca2+-Signaling and BADGE sex steroid progesterone, released in high amounts from the cumulus cells surrounding the oocyte (Lishko et al, 2011; Strünker et al, 2011). As we have shown that BADGE in μM concentrations can induce transient biphasic Ca2+ signals via an activation of CatSper in human sperm cells (Rehfeld et al, 2020), we hypothesized that a similar mechanism in the boar sperm cells could be responsible for the reproductive failure in sows. We set out to test this hypothesis, by investigating whether BADGE could interfere with Ca2+ signaling in boar sperm cells through an examination of the effect of both BADGE and the endogenous ligand of human CatSper, progesterone, on human and boar sperm cells side-by-side using a Ca2+ fluorimetric assay
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