The ethane dimethanesulfonate-induced decrease in the fertilizing ability of cauda epididymal sperm is independent of...

Area of Science:

• Reproductive Biology
• Toxicology
• Spermatology

Background:

• Ethane dimethanesulfonate (EDS) exposure in male rats was previously linked to reduced litter size.
• EDS has demonstrated effects on the epididymis independent of serum testosterone (T) levels.
• Prior research indicated EDS can directly affect epididymal epithelial cells in vitro.

Purpose of the Study:

• To investigate whether EDS exposure directly affects the fertilizing ability of sperm from the cauda epididymis.
• To determine the role of androgens and the testis in EDS-induced alterations of sperm fertilizing capacity.
• To identify potential biomarkers correlating with compromised sperm fertilizing ability after EDS exposure.

Main Methods:

• Adult male rats were exposed to ethane dimethanesulfonate (EDS) or sham treatment.
• In utero insemination of proximal cauda epididymal sperm was performed 4 days post-exposure.
• Fertilizing ability was assessed, alongside sperm motion, serum/epididymal T levels, and sperm protein analysis.

Main Results:

• Both castration and EDS exposure significantly reduced the fertilizing ability of proximal cauda epididymal sperm.
• Exogenous testosterone restored fertilizing ability after castration but not after EDS exposure.
• EDS's detrimental effects on sperm fertilizing ability were independent of testicular function and androgen status.

Conclusions:

• Ethane dimethanesulfonate (EDS) directly impairs sperm fertilizing ability in a manner independent of the testis.
• The findings highlight a specific mechanism of EDS toxicity on sperm maturation within the epididymis.
• An acidic 18-kDa sperm protein emerged as a potential indicator of compromised fertilizing capacity.