Thein vitroeffects of 2representative mycotoxins，T-2toxin and deoxynivalenol（DON），of trichothene group on the electron transport system（ETS）of mitochondria in rat cardiomyocytes were investigated by measuring oxygen consumption rates（OCR）。The ATP-linked OCR and the reserve capacity（RC）of the mitochondria ETS were quantified bya“mitochondria stress test”which was estimated by the OCR responses to oligomycin and carbonyl cyanide-p-trifluoromethoxyphenylhydrazone，with an extracellular flux analyzer.The basal OCR was significantly inhibited by the application of T-2 toxin at concentrations of 6×10^-1to 6×10^-5μM and DON at concentrations of 0.78 to 100μM for 24hr.The threshold of cardiomyocyte toxicity was estimated to be between6.0×10^-6and 6.0×10^-5μM for T-2 toxicity on both ATP-linked OCR and RC and between0.39and0.78μM on ATP-linked OCR or between1.56and3.13μM on RC for DON.The decrease in OCR of cardiomyocytes exposed to T-2 toxin with a concentration of 6.0×10^-3and，and 6.0×10^-4μMwas significantly inhibited by antioxidants，catalase and vitamin C.In conclusion，the present study demonstrated，through the direct and real-time measurement of respiratory function in mitochondria， that a marked inhibition of mitochondrial ETS function in cardiomyocytes was induced by T-2 toxin and DON and that the mitochondrial dysfunction by T-2 toxin was largely associated with oxidative stress。