Antifertility effects of an LHRH agonist in male mice

R Kher1, N R Kalla

  • 1Centre for Endocrine Sciences, Sanjay Gandhi PG Institute of Medical Sciences, Lucknow, India.

Contraception
|May 1, 1996
PubMed

Insights

High doses of a gonadotropin-releasing hormone agonist caused significant damage to mouse seminiferous epithelium and spermatogenesis. This led to reduced sperm motility and fertility, though complete azoospermia was not observed.

Area of Science:

  • Reproductive Biology
  • Toxicology
  • Endocrinology

Background:

  • Luteinizing hormone-releasing hormone (LHRH) agonists are used in various therapeutic applications.
  • Understanding their impact on male reproductive organs is crucial for safety assessments.

Purpose of the Study:

  • To investigate the effects of repeated high-dose LHRH agonist administration on the seminiferous epithelium of Swiss porton mice.
  • To assess the impact on spermatogenesis, sperm parameters, and fertility.

Main Methods:

  • Mice were administered repeated high doses of an LHRH agonist (1000 micrograms/kg wt/day).
  • Histological examination of seminiferous epithelium was performed.
  • Spermatogenesis, sperm motility, and fertility rates were evaluated.
  • Levels of the testis-specific enzyme lactate dehydrogenase C-X (LDH-X) were assessed.

Main Results:

  • Pronounced degenerative effects on seminiferous epithelium were observed, particularly at higher doses.
  • Spermatogenesis arrest occurred at all differentiation stages, becoming more evident after the pachytene spermatocyte stage.
  • A decrease in LDH-X levels correlated with a reduced number of gametogenic cells.
  • Acute inhibition of sperm motility was noted, leading to severely decreased fertility.
  • Reduced testosterone levels may have contributed to decreased libido and fertility.

Conclusions:

  • Repeated high-dose LHRH agonist treatment induces significant testicular toxicity and impairs spermatogenesis in mice.
  • The observed effects on sperm motility and potential impact on libido contribute to reduced fertility.
  • Further research is warranted to understand the long-term consequences and potential reversibility.

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