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Reduction of spermatogenesis and steroidogenesis in mice after fentin and fenbutatin administration
P Sreedhar Reddy1, T Pushpalatha, P Sreenivasula Reddy
1Department of Biotechnology, S.V. University, Tirupati 517502, India.
Abstract:
The present study was designed to assess potential reproductive toxicity caused by fentin and fenbutatin in the mice. Adult male mice received i.p. injections of fentin hydroxide and fenbutatin oxide at a dose of 0, 10 or 25 microg/kg body weight on 1st, 3rd and 5th day of experimentation. Mice were sacrificed on day 25 and analyzed for spermatogenesis and steroidogenesis. A significant decrease in epididymal sperm count, sperm motility, sperm viability and sperm function (HOS coiling) were observed in experimental mice when compared with controls. The decrease in sperm quantity and quality was significant in the 25 microg/kg group than that in the control group. The activity levels of testicular steroidogenic enzymes, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD) were significantly decreased in treated mice indicating decreased steroidogenesis after organotin compounds administration. The levels of serum testosterone decreased with an increase in follicle stimulating hormone and luteinizing hormone in experimental mice when compared to control mice. The results suggest that fentin and fenbutatin cause impairment of spermatogenesis through the inhibition of testosterone production.
Insights
Fentin and fenbutatin exposure significantly reduced sperm count, motility, and viability in male mice. These organotin compounds impaired spermatogenesis by decreasing testosterone production.
Area of Science:
- Reproductive Toxicology
- Environmental Health
- Endocrinology
Background:
- Organotin compounds like fentin and fenbutatin are used in agriculture.
- Potential reproductive toxicity of these compounds requires thorough investigation.
Purpose of the Study:
- To evaluate the reproductive toxicity of fentin hydroxide and fenbutatin oxide in adult male mice.
- To assess the impact of these organotins on spermatogenesis and steroidogenesis.
Main Methods:
- Adult male mice were administered intraperitoneal injections of fentin hydroxide and fenbutatin oxide at 0, 10, or 25 microg/kg.
- Spermatogenesis and steroidogenesis were analyzed on day 25 post-administration.
- Key parameters included epididymal sperm count, motility, viability, HOS coiling, testicular enzyme activity (3beta-HSD, 17beta-HSD), and serum hormone levels (testosterone, FSH, LH).
Main Results:
- Significant reductions in epididymal sperm count, motility, viability, and function were observed in treated mice.
- A dose-dependent decrease in sperm quantity and quality was noted, particularly in the 25 microg/kg group.
- Testicular steroidogenic enzyme activity (3beta-HSD and 17beta-HSD) significantly decreased, indicating impaired steroidogenesis.
- Serum testosterone levels were reduced, accompanied by increased FSH and LH levels in treated mice.
Conclusions:
- Fentin and fenbutatin exposure leads to significant impairment of spermatogenesis in male mice.
- These organotin compounds inhibit testosterone production, thereby affecting sperm parameters.
- The findings highlight the potential reproductive risks associated with fentin and fenbutatin exposure.
