Tamoxifen induces apoptosis and inhibits respiratory burst in equine neutrophils independently of estrogen receptors.

The research investigates how Tamoxifen, a nonsteroidal estrogen receptor modulator, affects equine neutrophils, the primary cells of the immune system. It shows that Tamoxifen has an impact on these cells independently from its interaction with estrogen receptors, reducing the neutrophils’ respiratory burst and increasing its early apoptosis, regardless of the presence of nuclear or membrane estrogen receptors.

Objective of the Research

• The research aims to investigate the effect of Tamoxifen on neutrophils in horses in vitro and how this effect is related to the action of tamoxifen on nuclear and membrane estrogen receptors in neutrophils.

Experiment Details

• The researchers firstly observed that Tamoxifen caused neutrophils to enter into early apoptosis, a process of programmed cell death, and inhibit respiratory burst, which is a rapid release of reactive oxygen species from different types of cells.
• They then tested whether these effects were due to Tamoxifen’s interaction with either of the two types of estrogen receptors present on neutrophils – nuclear (α and β) and membrane (GPR30).

Key Findings and Conclusion

• Tamoxifen was found to inhibit respiratory burst in neutrophils in a dose-dependent manner.
• Agonists and antagonists of nuclear and membrane estrogen receptors did not mimic or block the effect of Tamoxifen.
• The same was true for the increase in phosphatidylserine translocation, an early marker of apoptosis.
• This led to the conclusion that Tamoxifen’s effects on respiratory burst and early apoptosis are independent of its action on estrogen receptors in neutrophils.
• According to these findings, it can be concluded that the effects of Tamoxifen on respiratory burst and apoptosis in equine neutrophils are produced independently of the estrogen receptors present in these cells.
• Future research is required to understand how Tamoxifen leads to these effects, by investigating the drug’s interaction with other signaling pathways that may be involved in the process.

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