REACTIVE OXYGEN SPECIES TRIGGER THE FAST ACTION OF GLUFOSINATE

摘要

Glufosinate is classified as a contact, broad-spectrum and non-selective herbicide, causing plant tissue death within only a few hours after treatment. It is used in non-crop areas, orchards and vineyards, and for postemergence weed control in transgenic glufosinate-resistant soybean, canola, cotton and corn expressing a phosphinothricin acetyltransferase gene (Liberty Link, BASF). Commercialized as a synthetic mixture of d- and l-phosphinothricin, only the l-isomer has herbicidal activity, competingwith glutamate for the same binding site on GS (Bayer et al. 1972). This irreversible inhibition stops the conversion of glutamate into glutamine, causing up to 100-fold accumulation of ammonia (Wild et al. 1987).There is a definite association between the mechanism of action of glufosinate and its alteration of the photorespiration pathway (Wendler et al. 1992), with the effect of glufosinate on photosynthesis being higher under photorespiratory conditions (highlight intensity and warm temperature), and stronger on C3 species than C4 species (Wendler et al. 1990). However, the cascade of events leading to the extremely rapid glufosinate-induced foliar injury is still unclear.The effects of GS inhibition on ammonia accumulation and its consequence on carbon assimilation form the basis of our current understanding of the factors leading to plant death. However, our data challenge this paradigm by demonstrating that none of these factors are directly responsible for the light-dependent generation of reactive oxygen species (ROS) that leads to rapid cell death observed in plants treated with glufosinate. Consequently, the origin of the massive light-dependent production of ROSdriving the catastrophic lipid peroxidation of the cell membranes, and rapid cell death, must be reevaluated.