Trichothecene Mycotoxins Inhibit Mitochondrial Translation—Implication for the Mechanism of Toxicity

Toxins

Mohamed Anwar Bin-Umer²  John E. McLaughlin²  Debaleena Basu²  Susan McCormick¹ 

[1] Bacterial Foodborne Pathogens and Mycology Unit, National Center for Agricultural Utilization Research, United States Department of Agriculture, Agricultural Research Service, Peoria, IL 61604, USA;Department of Plant Biology and Pathology, School of Environmental and Biological Sciences, Rutgers University, New Brunswick, NJ 08901, USA;

关键词: trichothecenes;    deoxynivalenol;    T-2 toxin;    diacetoxyscirpenol;    Fusarium;    mitochondria;    ribosomes;    translation;    fusion;    Fission;    ROS;   

DOI  :  10.3390/toxins3121484

来源: mdpi

【 摘 要 】

Fusarium head blight (FHB) reduces crop yield and results in contamination of grains with trichothecene mycotoxins. We previously showed that mitochondria play a critical role in the toxicity of a type B trichothecene. Here, we investigated the direct effects of type A and type B trichothecenes on mitochondrial translation and membrane integrity in Saccharomyces cerevisiae. Sensitivity to trichothecenes increased when functional mitochondria were required for growth, and trichothecenes inhibited mitochondrial translation at concentrations, which did not inhibit total translation. In organello translation in isolated mitochondria was inhibited by type A and B trichothecenes, demonstrating that these toxins have a direct effect on mitochondrial translation. In intact yeast cells trichothecenes showed dose-dependent inhibition of mitochondrial membrane potential and reactive oxygen species, but only at doses higher than those affecting mitochondrial translation. These results demonstrate that inhibition of mitochondrial translation is a primary target of trichothecenes and is not secondary to the disruption of mitochondrial membranes.

【 授权许可】

CC BY   
© 2011 by the authors; licensee MDPI, Basel, Switzerland.