These authors contributed equally to this work.
Proteomic changes in chicken primary hepatocytes exposed to T-2 toxin are associated with oxidative stress and mitochondrial enhancement
Article first published online: 1 OCT 2013
© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Volume 13, Issue 21, pages 3175–3188, November 2013
How to Cite
Mu, P., Xu, M., Zhang, L., Wu, K., Wu, J., Jiang, J., Chen, Q., Wang, L., Tang, X. and Deng, Y. (2013), Proteomic changes in chicken primary hepatocytes exposed to T-2 toxin are associated with oxidative stress and mitochondrial enhancement. Proteomics, 13: 3175–3188. doi: 10.1002/pmic.201300015
Colour Online: See the article online to view Figs. 1, 2, and 4 in colour.
- Issue published online: 4 NOV 2013
- Article first published online: 1 OCT 2013
- Accepted manuscript online: 9 SEP 2013 02:01AM EST
- Manuscript Accepted: 9 AUG 2013
- Manuscript Revised: 5 AUG 2013
- Manuscript Received: 10 JAN 2013
- National Basic Research Program of China. Grant Number: 2009CB118802
- National Natural Science Foundation of China. Grant Number: 31172087
- Specialized Research Fund for the Doctoral Program of Higher Education of China. Grant Number: 20114404110010
- Guangdong Natural Science Foundation. Grant Number: S2012040007589
- China Postdoctoral Science Foundation. Grant Number: 2012M511577
- Mitochondrial enhancement;
- Oxidative stress;
- T-2 toxin
T-2 toxin is a mycotoxin that is toxic to plants, animals, and humans. However, its molecular mechanism remains unclear, especially in chickens. In this study, using 2D electrophoresis with MALDI-TOF/TOF-MS, 53 proteins were identified as up- or downregulated by T-2 toxin in chicken primary hepatocytes. Functional network analysis by ingenuity pathway analysis showed that the top network altered by T-2 toxin is associated with neurological disease, cancer, organismal injury, and abnormalities. Most of the identified proteins were associated with one of eight functional classes, including cell redox homeostasis, transcriptional or translational regulation, cell cycle or cell proliferation, stress response, lipid metabolism, transport, carbohydrate metabolism, and protein degradation. Subcellular location categorization showed that the identified proteins were predominantly located in the mitochondrion (34%) and interestingly, the expression of all the identified mitochondrial proteins was increased. Further cellular analysis showed that T-2 toxin was able to induce the ROS accumulation and could lead to an increase in mitochondrial mass and adenosine 5′-triphosphate content, which indicated that oxidative stress and mitochondrial enhancement occurred in T-2 toxin-treated cells. Overall, these results characterize the global proteomic response of chicken primary hepatocytes to T-2 toxin, which may lead to a better understanding of the molecular mechanisms underlying its toxicity.