Melatonin regulates mitochondrial enzymes and ascorbate-glutathione system during plant responses to drought stress through involving endogenous calcium

The study presented here was carried out to evaluate the effect of melatonin (Mel; N-acetyl-5-methoxytryptamine) on the arugula (Eruca sativa Mill.) plants grown under drought stress (DS). The results of the study show that DS significantly reduced the activity of mitochondrial ATP synthase and ATPase. Exposure of plants to DS caused a significant increase in the activity of NADPH oxidase and glycolate oxidase that resulted in the excess generation of superoxide (O-2(center dot-)) and hydrogen peroxide (H2O2) radicals, respectively. Creation of oxidative stress caused substantial damage to membrane lipids, leakage of electrolytes and reduced the hydration level of the drought-stressed plants. The damaging effects of DS were probably carried out because of lower activity of ATP synthase and ATPase, weak performance of antioxidant defense system and insufficient accumulation of osmolytes. Nevertheless, supplementation of drought stressed plants with 30 mu M Mel was remarkable in improving the activity of ATP synthase and ATPase with a concomitant activation of ascorbate-glutathione system, antioxidant enzymes, and accumulation of osmolytes. However, Mel inhibited the activity of NADPH oxidase and glycolate oxidase. This combined effect of events protected the plants from DS-induced impairments through reducing oxidative and osmotic stress as witnessed by a reduction in lipid peroxidation, electrolyte leakage and improvement in hydration status of the plants even under DS. On the contrary, inclusion of calcium (Ca2+) chelator overturned the positive effect of Mel on the stressed plants, that validates the involvement of endogenous Ca2+ during Mel-mediated plant adaptive responses to drought. The results of the study demonstrate that Mel involves Ca2+ in the orchestration of plant adaptive responses to DS by exerting regulatory control over the activity of mitochondrial enzymes and the function of the antioxidant defense system. (c) 2023 SAAB. Published by Elsevier B.V. All rights reserved.