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Updated: May 16, 2026

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Medium-throughput Screening Assays for Assessment of Effects on Ca2+-Signaling and Acrosome Reaction in Human Sperm
Published on: March 1, 2019
Effect of exposure to ulipristal acetate on sperm function
María José Munuce1, Carlos Zumoffen, Juliana Cicaré
1Laboratory of Reproductive Studies, Clinical Biochemistry Area, School of Biochemical and Pharmaceutical Sciences, National University of Rosario, Argentina.
Summary
Ulipristal acetate (UPA), used in emergency contraception, does not affect sperm vitality, protein tyrosine phosphorylation, or acrosome reaction. This suggests UPA is unlikely to impact sperm function following its use.
Area of Science:
- Reproductive biology
- Pharmacology
- Spermatozoa function
Background:
- Ulipristal acetate (UPA) is a key component of emergency contraception (EC).
- Spermatozoa may encounter UPA within the female reproductive tract after EC pill ingestion.
- Understanding UPA's effects on sperm function is crucial for reproductive health assessments.
Purpose of the Study:
- To investigate the impact of UPA exposure on essential sperm functions.
- To evaluate changes in sperm vitality, protein tyrosine phosphorylation (TyrP), and acrosome reaction (AR) upon UPA incubation.
Main Methods:
- Spermatozoa were incubated with varying concentrations of UPA (1-10,000 ng/ml) or a control medium.
- Key sperm parameters assessed included vitality, TyrP patterns, spontaneous AR, and human follicular fluid (hFF)-induced AR.
Main Results:
- Sperm vitality and TyrP patterns remained unchanged between UPA-exposed and control groups.
- Spontaneous acrosome reaction rates showed no significant difference.
- UPA did not inhibit the acrosome reaction induced by human follicular fluid.
Conclusions:
- UPA exposure at concentrations relevant to EC use did not alter sperm capacitation signaling (TyrP).
- UPA demonstrated no agonist effect on progesterone receptors, as it did not induce AR.
- UPA is unlikely to act as an antagonist on the acrosome reaction, as it did not prevent hFF-induced AR.
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