17β-estradiol modifies human spermatozoa mitochondrial function in vitro

Area of Science:

• Reproductive biology
• Mitochondrial physiology
• Endocrinology

Background:

• Spermatozoa are considered target cells for estrogens, but the precise mechanisms remain unclear.
• Understanding estrogenic effects on sperm is crucial for reproductive health research.

Purpose of the Study:

• To investigate the influence of 17β-estradiol (E2) on human spermatozoa mitochondrial function.
• To elucidate the dose-dependent effects of E2 on key sperm cellular processes.

Main Methods:

• Assessed intracellular calcium ion kinetics using Fluo-3.
• Measured mitochondrial membrane potential (ΔΨm) with JC-1 fluorochrome.
• Quantified mitochondrial superoxide anion production using MitoSOX RED dye.
• Evaluated sperm vitality and phosphatidylserine translocation via propidium iodide and annexin V staining, respectively.

Main Results:

• E2 induced a rapid, dose-dependent increase in intracellular calcium.
• A significant increase in high ΔΨm spermatozoa was observed at 10⁻⁸ M E2, but a decrease at 10⁻⁶ M E2.
• High E2 concentration (10⁻⁶ M) significantly elevated mitochondrial superoxide anion levels.
• Sperm vitality and membrane integrity remained unaffected after 2 hours of E2 exposure at all tested concentrations.

Conclusions:

• 17β-estradiol significantly affects human spermatozoa mitochondrial function.
• Low E2 concentrations appear to improve mitochondrial function, whereas high concentrations may impair it.
• These findings highlight a complex, dose-dependent role of E2 in regulating sperm bioenergetics and potential function.