Journal
JOURNAL OF ENVIRONMENTAL SCIENCES
Volume 26, Issue 4, Pages 917-925Publisher
SCIENCE PRESS
DOI: 10.1016/S1001-0742(13)60510-0
Keywords
T-2 toxin; developmental toxicity; apoptosis; zebrafish embryo; oxidative stress
Categories
Funding
- National Basic Research Program (973) of China [2011CB503803]
- National Key Project on Drug Development from the Ministry of Science and Technology of China [2009ZX09501-034]
- China Postdoctoral Science Foundation [20110491865]
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T-2 toxin is one of the most important trichothecene mycotoxins occurring in various agriculture products. The developmental toxicity of T-2 toxin and the exact mechanism of action at early life stages are not understood precisely. Zebrafish embryos were exposed to different concentrations of the toxin at 4-6 hours post fertilization (hpf) stage of development, and were observed for different developmental toxic effects at 24, 48, 72, and 144 hpf. Exposure to 0.20 mu mol/L or higher concentrations of T-2 toxin significantly increased the mortality and malformation rate such as tail deformities, cardiovascular defects and behavioral changes in early developmental stages of zebrafish. T-2 toxin exposure resulted in significant increases in reactive oxygen species (ROS) production and cell apoptosis, mainly in the tail areas, as revealed by Acridine Orange staining at 24 hpf. In addition, T-2 toxin-induced severe tail deformities could be attenuated by co-exposure to reduced glutathione (GSH). T-2 toxin and GSH co-exposure induced a significant decrease of ROS production in the embryos. The overall results demonstrate that T-2 toxin is able to produce oxidative stress and induce apoptosis, which are involved in the developmental toxicity of T-2 toxin in zebrafish embryos.
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