T-2 toxin induces apoptosis via the Bax-dependent caspase-3 activation in mouse primary Leydig cells

Area of Science:

• Toxicology
• Cell Biology
• Molecular Mechanisms

Background:

• Leydig cells are crucial for testosterone production in males.
• T-2 toxin is a mycotoxin with known toxic effects.
• Understanding T-2 toxin's impact on Leydig cells is important for reproductive health.

Purpose of the Study:

• To investigate the toxic effects of T-2 toxin on mouse Leydig cells.
• To elucidate the molecular mechanisms underlying T-2 toxin-induced cell damage.
• To assess T-2 toxin's impact on Leydig cell proliferation, apoptosis, and related gene expression.

Main Methods:

• Isolation and culture of primary mouse Leydig cells.
• Treatment of Leydig cells with varying concentrations and durations of T-2 toxin.
• Assessment of cell proliferation, mitochondrial activity, and apoptosis rates.
• Measurement of mRNA expression levels for apoptosis-related genes (Bcl-2, Bax, PARP, caspase-3).

Main Results:

• T-2 toxin inhibited Leydig cell proliferation at concentrations >10⁻⁹ M or time >12 h.
• T-2 toxin decreased Bcl-2 mRNA levels and mitochondrial activity (>10⁻⁹ M).
• T-2 toxin increased Bax (>10⁻⁸ M) and PARP (>10⁻⁹ M) mRNA expression, activating caspase-3 and inducing apoptosis.

Conclusions:

• T-2 toxin induces apoptosis in mouse Leydig cells through a mitochondria-mediated pathway.
• The mechanism involves the activation of Bax-dependent caspase-3.
• These findings highlight T-2 toxin's potential reproductive toxicity.