Triphenyltin Chloride Delays Leydig Cell Maturation During Puberty in Rats

Area of Science:

• Endocrinology
• Toxicology
• Reproductive Biology

Background:

• Triphenyltin chloride (TPT) is an environmental contaminant found in food.
• TPT is a suspected endocrine disruptor affecting Leydig cells, but its impact on pubertal development is unknown.

Purpose of the Study:

• To investigate the effects of TPT on pubertal Leydig cell development in rats.
• To elucidate the molecular mechanisms underlying TPT-induced disruption.

Main Methods:

• Male rats (35 days old) were exposed to TPT (0.5, 1, or 2 mg/kg/day) for 18 days.
• Immature Leydig cells were treated with TPT (10 and 100 nM) *in vitro*.
• Serum testosterone, gene expression (Star, Lhcgr, Cyp11a1, Hsd3b1, Hsd17b3), protein phosphorylation (AKT1, AKT2, ERK1/2), ROS production, and apoptosis were analyzed.

Main Results:

• TPT exposure *in vivo* (≥0.5 mg/kg) reduced serum testosterone and Star mRNA levels.
• Higher TPT doses (2 mg/kg) decreased Lhcgr, Cyp11a1, Hsd3b1, Hsd17b3 mRNA and reduced AKT/ERK phosphorylation.
• *In vitro* TPT (100 nM) increased reactive oxygen species (ROS) and Leydig cell apoptosis.

Conclusions:

• TPT exposure disrupts pubertal Leydig cell development and function.
• Mechanisms involve reduced steroidogenic enzyme expression and impaired AKT/ERK signaling pathways.
• TPT induces oxidative stress and apoptosis in immature Leydig cells.