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Updated: Jan 13, 2026

Medium-throughput Screening Assays for Assessment of Effects on Ca2+-Signaling and Acrosome Reaction in Human Sperm
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Clonidine compromises human sperm functions.

Xuchang Liu1, Yanfan Cui2, Ruirui Qian2

  • 1Queen Mary School, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi 330031, China.

Reproductive Toxicology (Elmsford, N.Y.)
|January 10, 2026
PubMed
Summary
This summary is machine-generated.

Clonidine affects male fertility by interfering with sperm function. While low doses preserve sperm, higher doses are toxic, and it inhibits key fertilization signaling pathways.

Keywords:
Calcium signalingCatSper channelClonidineMitochondrial membrane potentialProgesteroneSperm

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Area of Science:

  • Reproductive Biology
  • Pharmacology
  • Andrology

Background:

  • Clonidine is a common medication for hypertension and ADHD.
  • Its effects on male fertility are largely unknown.
  • Understanding these effects is crucial for reproductive health.

Purpose of the Study:

  • To investigate clonidine's impact on human sperm function.
  • To analyze its effects on progesterone-induced signaling pathways.
  • To determine potential mechanisms affecting male fertility.

Main Methods:

  • Human sperm exposed to varying clonidine concentrations (6.25-200μM).
  • Assessed viability, motility (CASA), calcium signaling, electrophysiology, mitochondrial potential, ROS, capacitation, and protein phosphorylation.
  • Utilized eosin staining, chlortetracycline staining, and Western blot.

Main Results:

  • Clonidine showed biphasic effects: ≤50μM preserved viability/motility, ≥100μM caused cytotoxicity.
  • Potently inhibited progesterone-induced calcium signaling, capacitation, and acrosome reaction.
  • Partially enhanced CatSper channel activity, affecting ~50% of calcium responses.

Conclusions:

  • Clonidine selectively interferes with progesterone-mediated sperm responses.
  • It preserves baseline sperm functions while disrupting fertilization signaling.
  • Findings suggest a novel mechanism impacting male fertility in vitro, requiring further clinical investigation.