▪ Abstract To cope with environmental fluctuations and to prevent invasion by pathogens, plant metabolism must be flexible and dynamic. Active oxygen species, whose formation is accelerated under stress conditions, must be rapidly processed if oxidative damage is to be averted. The lifetime of active oxygen species within the cellular environment is determined by the antioxidative system, which provides crucial protection against oxidative damage. The antioxidative system comprises numerous enzymes and compounds of low molecular weight. While research into the former has benefited greatly from advances in molecular technology, the pathways by which the latter are synthesized have received comparatively little attention. The present review emphasizes the roles of ascorbate and glutathione in plant metabolism and stress tolerance. We provide a detailed account of current knowledge of the biosynthesis, compartmentation, and transport of these two important antioxidants, with emphasis on the unique insights and advances gained by molecular exploration.

Efficient flux through plant electron transport cascades requires the simultaneous presence of both oxidized and reduced forms of electron carriers. This requirement, known as redox poising, involves a continuous flux of electrons to molecular oxygen from multiple sites in the photosynthetic and respiratory electron transport chains. Apart from the specialized water-producing reactions catalyzed by specific oxidases, the initial product of this flux is superoxide, from which other ROS are subsequently produced (Table 1). Singlet oxygen is also formed during light capture and photochemistry. Numerous enzyme systems produce superoxide or H₂O₂. The reactive nature of these intermediates means not only that their accumulation must be controlled but also that they are able to act as signaling molecules.

While the chemical nature of reactive oxygen species (ROS) dictates that they are potentially harmful to cells, recent genetic evidence suggests that in planta purely physicochemical damage may be much more limited than previously thought. The most potentially deleterious effect of ROS under most conditions is that at high concentrations they trigger genetically programmed cell suicide events. Moreover, because plants use ROS as second messengers in signal transduction cascades in processes as diverse as mitosis, tropisms and cell death, their accumulation is crucial to plant development as well as defence. Direct ROS signal transduction will ensue only if ROS escape destruction by antioxidants or are otherwise consumed in a ROS cascade. Thus, the major low molecular weight antioxidants determine the specificity of the signal. They are also themselves signal‐transducing molecules that can either signal independently or further transmit ROS signals. The moment has come to re‐evaluate the concept of oxidative stress. In contrast to this pejorative or negative term, implying a state to be avoided, we propose that the syndrome would be more usefully described as ‘oxidative signalling’, that is, an important and critical function associated with the mechanisms by which plant cells sense the environment and make appropriate adjustments to gene expression, metabolism and physiology.