T-2 toxin induces apoptosis via the Bax-dependent caspase-3 activation in mouse primary Leydig cells |
| |
| Authors: | Yong Fa Zhang Pan Ke Su Lun Ji Wang Hui Qi Zheng Xue Fei Bai Ping Li |
| |
| Affiliation: | 1. College of Medical Technology and Engineering, Henan University of Science and Technology, Luoyang, China;2. College of Food and Bioengineering, Henan University of Science and Technology, Luoyang, China;3. The First Affiliated Hospital and College of Clinical Medicine, Henan University of Science and Technology, Luoyang, China;4. College of Food and Bioengineering, Henan University of Science and Technology, Luoyang, China |
| |
| 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 |
|
|
