| Many studies have been done on the effects of Alternaria alternata on plants, but little is known about the characteristics and mechanisms of the programmed cell death (PCD) induced by Alternaria alternata metabolic products (MP), and the effect of the Alternaria alternata metabolic products on the mitochondria respiration and the relationship between the mitochondria respiration and PCD have not been known yet. Tobacco BY-2 cell is a cell line without functional chloroplasts. The BY-2 cell was used in this study to explore the mechanism of the PCD induced by the MP without influence of reactive oxygen species (ROS) mediated by photosynthetic electron transport.The main results obtained are as follow: Treatment with the MP led to remarkable cell death which was proved to be PCD as indicated by occurring of cytoplasm shrinkage, chromatin condensation and DNA laddering in the cells. Moreover, the MP treatment resulted in overproduction of reactive oxygen species, a rapid depletion of ATP and a decline of respiration in tobacco BY-2 cells. Furthermore, it was demonstrated that the direct inhibition of mitochondria electron transport chain (ETC), alternative oxidase (AOX) pathway capacity and CAT activity by MP treatment might be the main contributors to the MP-induced ROS burst in tobacco BY-2 cells. Addition of adenosine significantly inhibited the ATP depletion induced by the MP without preventing the PCD, however, addition of commercial calalase (CAT) significantly blocked ROS overproduction induced by the MP, which prevented the occurring of the PCD in the MP treated BY-2 cells.The data presented here demonstrate that the ROS burst was more correlated with the MP-induced PCD than ATP depletion in the tobacco BY-2 cells. The results provided evidences that the Alternaria alternata metabolic products could induce PCD, which was accompanied by ROS burst, ATP depletion and respiration decline in tobacco BY-2 cells.
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