The antioxidant systems vis-à-vis reactive oxygen species during plant–pathogen interaction

• Published in: Plant Physiology and Biochemistry Vol. 41; no. 10; pp. 863 - 870
• Main Authors: De Gara, Laura, de Pinto, Maria C., Tommasi, Franca
• Format: Book Review Journal Article
• Language: English
• Published: Elsevier Masson SAS 01-10-2003
• Subjects: Antioxidants; Ascorbate; Glutathione; Hypersensitive response; Plant–pathogen interaction; Reactive oxygen species; Redox regulation; Plant–pathogen interaction; GSSG; NO; Reactive oxygen species; Hypersensitive response; Redox regulation; APX; SOD; Ascorbate; HR; SA; Antioxidants; PCD; ASC; CAT; ROS; DHA; TMV; GSH; Glutathione
• ISSN: 0981-9428; 1873-2690
• DOI: 10.1016/S0981-9428(03)00135-9

Plant resistance to pathogens requires the activation of complex metabolic pathways in the infected cells, aimed at recognizing pathogen presence and hindering its propagation within plant tissues. In spite of this both compatible and incompatible responses induce alterations in plant metabolism, only in the latter the plant is able to efficiently block pathogen penetration without suffering excessive damage. One of the most studied incompatible responses is based on the hypersensitive response (HR), in which cells surrounding the site of pathogen penetration switch on genes encoding for phytoalexin synthesis and other pathogenesis related proteins before activating programmed cell death (PCD). The production of reactive oxygen species (ROS) is a key event in HR. Several enzymatic systems have been proposed to be responsible for the oxidative burst characterizing HR. In this review, the involvement of antioxidant redox systems, in particular those related to ascorbate (ASC) and glutathione (GSH), in activating both compatible and incompatible plant responses is analysed. Increasing lines of evidence indicate that alterations in the levels and/or redox state of ASC and/or GSH, as well as in the activity of their redox enzymes, occur during the HR programme. These alterations do not seem to be a mere consequence of the oxidative stress induced by the massive ROS production, but they are induced as part of the transduction pathways triggering defence responses and PCD. The possibility that ASC and GSH systems are links in a redox signalling chain activating defence strategies is also discussed.