Low concentrations of lead decrease the sperm fertilization ability by altering the acrosome reaction in mice.

Area of Science:

• Reproductive Toxicology
• Environmental Health
• Sperm Biology

Background:

• Lead (Pb) exposure is linked to adverse effects on sperm quality and fertilization.
• Sperm capacitation and acrosome reaction (AR) are critical for fertilization.
• Actin polymerization, regulated by small GTPases like RhoA, Rac1, and Cdc42, is essential for these processes.

Purpose of the Study:

• To investigate the impact of low-level lead exposure on mouse sperm fertilization ability.
• To examine the effects of lead on sperm capacitation, acrosome reaction, and actin polymerization.
• To elucidate the role of RhoA, Rac1, and Cdc42 in lead-induced sperm dysfunction.

Main Methods:

• Mice were exposed to 0.01% Pb²⁺ in drinking water for 45 days.
• Spermatozoa were analyzed for acrosome reaction (AR), sperm capacitation (P-Tyr), actin polymerization, MDA levels, and Rho GTPase protein expression.
• In vitro fertilization (IVF) assays were performed to assess fertilization rates.

Main Results:

• Blood lead levels reached 9.4 ± 1.6 μg/dL.
• Increased oAR (19%) and abnormal sperm morphology, but decreased induced AR (iAR) (15%).
• Significant reductions in actin polymerization (sperm head 59%, tail 42%) and Rac1 protein levels (33%), leading to a 19% decrease in fertilization rate.

Conclusions:

• Lead exposure at environmental concentrations (PbB < 10 μg/dL) impairs sperm function and fertilization.
• Reduced Rac1 levels appear to be a key mechanism, hindering adequate actin polymerization.
• This dysfunction affects acrosome reaction and overall sperm fertilizing capacity.