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

Abstract

To explore the toxic effect of T-2 toxin on mouse Leydig cells and its underlying molecular mechanisms, we isolated Leydig cells from mature mice, set-up Leydig cells culture, treated cells with T-2 toxin, evaluated cell proliferation, detected the caspase-3 activity, mitochondrial activity and apoptosis rate, and measured the mRNA levels of Bcl-2, Bax, PARP and caspase-3. T-2 toxin inhibited cell proliferation at concentrations higher than 10⁻⁹ M or time more than 12 h, T-2 toxin also decreased Bcl-2 expression at the mRNA levels and mitochondrial activity at concentrations higher than 10⁻⁹ M. While, T-2 toxin increased the mRNA expressions of Bax and PARP at concentrations higher than 10⁻⁸ M and 10⁻⁹ M, respectively, triggered mitochondria-mediated apoptosis, activated downstream caspase-3, and then increased caspase-3 at the activity and mRNA levels at concentrations higher than 10⁻⁹ M. These data showed that T-2 toxin appears to activate specific intracellular death-related pathways leading to Bax-dependent caspase-3 activation and the induction of apoptosis in Leydig cells.

Keywords:

• T-2 toxin
• Leydig cells
• apoptosis
• activity
• mRNA

Disclosure statement

The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.

Additional information

Funding

This work was supported by the Natural Science Foundation of China (31201119), the China Scholarship Council Foundation (201408410288) and Henan Youth Backbone Teacher of University Foundation (2013GGJS-067).