Apoptosis regulator BAX
response to toxic substance
T-2 toxin induces apoptosis, and selenium partly blocks, T-2 toxin induced apoptosis in chondrocytes through modulation of the Bax/Bcl-2 ratio.
T-2 toxin is one of the mycotoxins, a group of type A trichothecenes produced by several fungal genera including Fusarium species. In the present study, we have investigated the apoptotic effects of T-2 toxin on chondrocytes and the relationship between T-2 toxin induced chondrocyte apoptosis and its influence on Bcl-2/Bax protein and mRNA expression. We have also examined the inhibitory effects of selenium on chondrocyte apoptosis induced by T-2 toxin. We have combined morphological and biological techniques to establish the relevance of apoptosis in human chondrocyte death induced by T-2 toxin. Treatment with T-2 toxin caused accelerated apoptosis in a concentration dependent manner. The apoptosis induced by T-2 toxin involved an increased Bax/Bcl-2 ratio. Bcl-2 mRNA expression remained unchanged in chondrocyte apoptosis induced by T-2 toxin treatment, while Bax mRNA expression increased following treatment with T-2 toxin. Selenium could partly block the apoptosis of chondrocytes induced by T-2 toxin through decreasing the Bax/Bcl-2 ratio. These results suggest that, under our experimental conditions, apoptosis of chondrocytes can be induced by T-2 toxin (1-20ng/mL) via the Bcl-2 and Bax proteins, and the Bax/Bcl-2 ratio may play a critical role in governing the susceptibility to apoptosis induced by T-2 toxin in human chondrocytes.