Nitric oxide and phytohormone interactions in the response of Lactuca sativa to salinity stress.

MAIN CONCLUSION: Nitric oxide increased lettuce's tolerance to salinity by restoring its hormonal balance, consequently reducing Na + accumulation and activating defense mechanisms that allowed the attenuation of ionic, oxidative, and osmotic stresses. Agricultural crops are continually threatened by soil salinity. The plant's ability to tolerate soil salinity can be increased by treatment with the signaling molecule nitric oxide (NO). Involvement of NO in plant metabolism and its interactions with phytohormones have not been fully described, so knowledge about the role of this radical in signaling pathways remains fragmented. In this work, Lactuca sativa (lettuce) plants were subjected to four treatments: (1) control (nutrient solution); (2) SNP [nutrient solution containing 70 µM sodium nitroprusside (SNP), an NO donor]; (3) NaCl (nutrient solution containing 80 mM NaCl); or (4) SNP + NaCl (nutrient solution containing SNP and NaCl). The plants were exposed to these conditions for 24 h, and then, the roots and leaves were collected and used to evaluate biochemical parameters (reactive oxygen species (ROS) production, cell membrane damage, cell death, antioxidant enzymes activities, and proline concentration), physiological parameters (pigments' concentration and gas-exchange measurements), and phytohormone content. To evaluate growth, tolerance index, and nutrient concentration, the plants were exposed to the treatments for 3 days. L sativa exposure to NaCl triggered ionic, osmotic, and oxidative stress, which resulted in hormone imbalance, cell death, and decreased growth. These deleterious changes were correlated with Na+ content in the vegetative tissues. Adding NO decreased Na+ accumulation and stabilized the mineral nutrient concentration, which maintained the photosynthetic rate and re-established growth. NO-signaling action also re-established the phytohormones balance and resulted in antioxidant system activation and osmotic regulation, with consequent increase in plants tolerance to the salt.

Corrigendum: The Involvement of Nitric Oxide in Integration of Plant Physiological and Ultrastructural Adjustments in Response to Arsenic.

[This corrects the article on p. 516 in vol. 8, PMID: 28469622.].

The Involvement of Nitric Oxide in Integration of Plant Physiological and Ultrastructural Adjustments in Response to Arsenic.

High arsenic (As) concentrations are toxic to all the living organisms and the cellular response to this metalloid requires the involvement of cell signaling agents, such as nitric oxide (NO). The As toxicity and NO signaling were analyzed in Pistia stratiotes leaves. Plants were exposed to four treatments, for 24 h: control; SNP [sodium nitroprusside (NO donor); 0.1 mg L-1]; As (1.5 mg L-1) and As + SNP (1.5 and 0.1 mg L-1, respectively). The absorption of As increased the concentration of reactive oxygen species and triggered changes in the primary metabolism of the plants. While photosynthesis and photorespiration showed sharp decrease, the respiration process increased, probably due to chemical similarity between arsenate and phosphate, which compromised the energy status of the cell. These harmful effects were reflected in the cellular structure of P. stratiotes, leading to the disruption of the cells and a possible programmed cell death. The damages were attenuated by NO, which was able to integrate central plant physiological processes, with increases in non-photochemical quenching and respiration rates, while the photorespiration level decreased. The increase in respiratory rates was essential to achieve cellular homeostasis by the generation of carbon skeletons and metabolic energy to support processes involved in responses to stress, as well to maintaining the structure of organelles and prevent cell death. Overall, our results provide an integrated view of plant metabolism in response to As, focusing on the central role of NO as a signaling agent able to change the whole plant physiology.