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. 2023 Jun 30;64:102805. doi: 10.1016/j.redox.2023.102805

Fig. 5.

Fig. 5

Systematic model explaining the interaction of reactive oxygen species (ROS) and reactive nitrogen species (NOS) with melatonin (MT). (1) The environmental stresses induce alternation in the redox balance. (2) Increasing ROS/RNS levels causes oxidative/nitrosative stress. (3)The redox imbalance triggers the MT biosynthetic genes to produce (4) MT. (5) The MT triggers its receptor (CAND/PMTR1) to induce changes in (6) NOS-like enzyme and NR, which elevates the NO levels and antioxidant (CAT, SOD, APX, GPX, PRX) levels. (7) Consequently, these enzymes degrade the ROS species to stabilize cellular homeostasis. (8) The direct action of MT (and its byproducts) also inhibits the increased level of ROS/RNS. (9) The regulation of NO via interaction of its biosynthesis enzymes with MT and with O2·- to form ONOO triggers the signaling cascade response. (10) The MT triggers other phytohormones to interact with NO signaling to activate plant defense response. ASA: ascorbic acid; GSH: glutathione; RbOH: respiratory burst oxidase homolog; GPX: glutathione peroxidase; SOD: superoxide dismutase; NR: nitrate reductase; NOS: nitric oxide synthase; CAT: catalase; PRX: peroxiredoxin.