Reproduction Abstracts

Background: The sperm require energy-intensive motility to reach the female gamete for delivering the male genome. This energy is conserved by keeping the sperm quiescent in cauda epididymis before ejaculation, but the molecular mechanisms controlling this unique process remain an enigma. Cauda sperm produce H₂O₂, and we have attempted to study the redox regulation of sperm motility.

Methods: Quiescent and motile sperm were collected from Sprague Dawley rat cauda epididymides and experimented in vitro. Care was taken to prevent motility initiation of quiescent sperm on isolation from epididymis.

Results: Free thiols on quiescent sperm increased by ~2-fold on motility initiation. Caudal sperm failed to initiate motility in presence of 0.1% sulfhydryl-alkylating agent N-ethylmaleimide (NEM), and when applied vaginally before mating 50 mg NEM prevented pregnancy in rabbits. While ~50% motile-sperm lost complete motility when placed in0.05% H₂O₂, 50% quiescent-sperm did not initiate any motility at 0.02% H₂O₂. Similarly, all motile sperm could be immobilized by at least 2.0% H₂O₂ while none of the quiescent sperm could initiate motility at 0.25% H₂O₂. However, caudal sperm could initiate good motility at pH (6.85) and viscosity (82 cP) of the caudal semen.

Conclusions: The redox potential of sperm thiols may play a crucial role in rat sperm quiescence and motility initiation. The pH and viscosity of caudal semen may not have a critical effect on sperm motility suppression. Quiescent sperm are more susceptible to these factors than motile sperm.