Melatonin–Nitric Oxide Interaction Modulates Catalase Activity and Hydrogen Peroxide Homeostasis in Sunflower Seedling Cotyledons Accompanying NaCl Stress

Modulation of catalase activity can be one of the probable adaptive mechanisms in plants to alleviate stress by regulating intracellular hydrogen peroxide (H 2 O 2 ) levels. Catalase is expected to exhibit affinity for nitric oxide (NO) since heme iron is its intrinsic constituent. Melatonin, a tryptophan derivative, can also be expected to regulate catalase activity through its interaction with NO, direct scavenging of H 2 O 2 , or inhibition of NO biosynthesis. A crosstalk between melatonin and NO has been investigated in sunflower seedlings subjected to 120 mM NaCl in the presence of NO donor (Diethylenetriamine NONOate (DETA)) and/or melatonin through changes in catalase activity and H 2 O 2 levels. Confocal laser scanning microscopy (CLSM) imaging of catalase in the cells of seedling cotyledons and spectrofluorometric estimation of endogenous NO in the tissue have also been undertaken. A significant upregulation of catalase activity by melatonin in sunflower seedling cotyledons, more so in salt-stressed conditions, is evident. NO and melatonin show an inverse relationship in altering catalase activity. Melatonin brings about a decrease in endogenous NO content in seedling cotyledons in salt stress conditions. NO binding with ferric heme moiety presumably results in the formation of ferric–nitrosyl complex which prevents H 2 O 2 binding to ferric ion, thereby inhibiting catalase activity. NO may also interact with some constituents of oil body membrane, like caleosins and oleosins, thereby affecting the rate of oil body degradation under salt stress. NO–melatonin interaction is thus evident in the regulation of H 2 O 2 homeostasis and catalase activity distribution as a long-distance signaling response to salt stress.