Interactions between salicylic acid and antioxidant enzymes tilting the balance of HO from photorespiration in non-target crops under halosulfuron-methyl stress.

Halosulfuron-methyl (HSM) is a safe, selective and effective sulfonylurea herbicide (SU) for the control of sedge and broadleaf weeds in sugarcane, corn, tomato, and other crops. The primary site of action is acetolactate synthase (ALS), a key enzyme of branched chain amino acids (BCAAs) synthesis. In addition to ALS inhibition, BCAAs deficiencies and oxidative damage may be involved in toxic effects of SUs. However, secondary targets of HSM relevant to plant physiological responses are unclear. In the present study, comparative growth inhibition and peroxidization injury between sensitive and tolerance crops were observed at biochemical and physiological levels suggesting involvement of HO, ethylene, salicylic acid (SA) in the oxidative stress responses to HSM. HSM caused accumulation of HO, stimulated photorespiration and consequent accumulation of SA that worsened the peroxidization injury to the sensitive C plant soybean (Glycine max). The growth inhibition at low concentrations of HSM could be lessened by supplementary BCAAs, reactive oxygen species scavengers or ethylene inducers, whereas the oxidation damage at high concentrations of HSM could not be reversed and ultimately lead to plant death. HO at a low level stimulated the antioxidase system including glutathione S-transferase activities in the HSM-tolerant C maize (Zea mays), which contributes to HSM tolerance. HO plays an important role on HSM stress responses in both HSM-sensitive and HSM-tolerant soybean and maize.