T-2 toxin induces apoptosis, and selenium partly blocks, T-2 toxin induced apoptosis in chondrocytes through modulation of the Bax/Bcl-2 ratio
Autor: | Zhi-lun Wang, Jun-ling Cao, Yong-lie Chu, Jinghong Chen, Zhan-tian Yang, Xiong Guo |
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Rok vydání: | 2006 |
Předmět: |
Programmed cell death
Gene Expression Apoptosis Biology Toxicology Inhibitory postsynaptic potential medicine.disease_cause Chondrocyte Flow cytometry Selenium Chondrocytes medicine Humans RNA Messenger Dose-Response Relationship Drug medicine.diagnostic_test Reverse Transcriptase Polymerase Chain Reaction Toxin RNA General Medicine Flow Cytometry Molecular biology T-2 Toxin Dose–response relationship medicine.anatomical_structure Proto-Oncogene Proteins c-bcl-2 Food Science |
Zdroj: | Food and Chemical Toxicology. 44:567-573 |
ISSN: | 0278-6915 |
DOI: | 10.1016/j.fct.2005.09.004 |
Popis: | 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. |
Databáze: | OpenAIRE |
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