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Inhibitory effect of tributyltin on expression of steroidogenic enzymes in mouse testis
Suel-Kee Kim1, Jong-Hoon Kim, Jung Ho Han
1Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
Abstract:
Tributyltin (TBT) is known to disrupt the development of reproductive organs, thereby reducing fertility. The aim of this study was to evaluate the acute toxicity of TBT on the testicular development and steroid hormone production. Immature (3-week-old) male mice were given a single administration of 25, 50, or 100 mg/kg of TBT by oral gavage. Lumen formation in seminiferous tubule was remarkably delayed, and the number of apoptotic germ cells found inside the tubules was increased in the TBT-exposed animals, whereas no apoptotic signal was observed in interstitial Leydig cells. Reduced serum testosterone concentration and down-regulated expressions of the mRNAs for cholesterol side-chain cleavage enzyme (P450scc), 17alpha -hydroxylase/C(17-20) lyase (P450(17alpha)), 3beta -hydroxysteroid-dehydrogenase (3beta -HSD), and 17beta -hydroxysteroid-dehydrogenase (17beta -HSD) were also observed after TBT exposure. Altogether, these findings demonstrate that exposure to TBT is associated with induced apoptosis of testicular germ cells and inhibition of steroidogenesis by reduction in the expression of steroidogenic enzymes in interstitial Leydig cells. These adverse effects of TBT would cause serious defects in testicular development and function.
Insights
Tributyltin (TBT) exposure in young mice delayed reproductive organ development and reduced fertility. TBT increased germ cell death and inhibited steroid hormone production, impairing testicular function.
Area of Science:
- Environmental Toxicology
- Reproductive Toxicology
- Endocrinology
Background:
- Tributyltin (TBT) is an organotin compound recognized for its endocrine-disrupting properties.
- TBT exposure is linked to adverse effects on reproductive system development and function, impacting fertility.
Purpose of the Study:
- To investigate the acute toxic effects of TBT on testicular development in immature male mice.
- To assess the impact of TBT on steroid hormone production and the expression of key steroidogenic enzymes.
Main Methods:
- Immature male mice received single oral doses of TBT (25, 50, or 100 mg/kg).
- Evaluated testicular histology, including seminiferous tubule lumen formation and germ cell apoptosis.
- Measured serum testosterone levels and the mRNA expression of steroidogenic enzymes (P450scc, P45017α, 3β-HSD, 17β-HSD).
Main Results:
- TBT exposure significantly delayed seminiferous tubule lumen formation and increased germ cell apoptosis.
- A notable decrease in serum testosterone concentrations was observed post-TBT exposure.
- Down-regulation of mRNA expression for key steroidogenic enzymes (P450scc, P45017α, 3β-HSD, 17β-HSD) in Leydig cells was evident.
Conclusions:
- Acute TBT exposure induces testicular germ cell apoptosis and inhibits steroidogenesis by reducing steroidogenic enzyme expression.
- These effects contribute to significant defects in testicular development and function, potentially leading to reduced fertility.
