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Early reports that plants have the capacity to generate NO did not attract the attention of plant physiologists for many years, until 1987 when NO was identified by Prof. Moncada's group as the endothelium-derived relaxing factor in mammals. Plant physiologists and biochemists have started to pay attention to this gas and today NO is known as a versatile molecule with multiple functions in several complex processes such as seed germination, development, senescence, and defence against biotic/abiotic stress. This chapter presents an overview of the present knowledge on the involvement of NO and other reactive nitrogen species in plant abiotic stress, with special emphasis on nitrosative stress as a new component of plant stress physiology.

Growing evidence suggests that nitric oxide (NO) is a central molecule in several physiological functions, ranging from plant development to defence responses. Plants use NO as a signaling molecule in pathways comparable to those of mammals, suggesting the existence of many commonalities between the action of NO in plants and animals.

In this chapter, we examine the mechanisms through which plants respond to pathogen challenge and focus on inherent NO signaling functions. In particular, we describe the major NO-generating systems and their involvement in the response to pathogen attack, the role of NO in the activation of the hypersensitive response (HR), and the participation in the establishment of systemic acquired resistance (SAR). Next we describe the evidence for the involvement of Ca, cyclic GMP (cGMP), cyclic ADP-ribose (cADPR), and mitogen-activated protein kinases (MAPK) in NO-mediated signal cascades, the role of NO in posttransational protein modifications, and its participation in modulating gene expression.

The primary and probably only important role that NO plays in the hypersensitive response is communication between dying cells and neighboring cells. NO accumulates extracellularly immediately prior to programmed cell death of infected cells and inhibits extracellular HO-degrading enzymes, leading to HO accumulation. NO and/or HO travel to adjacent cells, where HO accumulation induces salicylic acid biosynthesis. Salicylic acid mediates the observed NO-dependent potentiation of programmed cell death triggering. These effects appear to depend upon augmentation of plasma membrane depolarization by direct effects of salicylic acid; whereas delayed negative feedback on programmed cell death is gene expression-dependent.

Nitric oxide () is an important signaling molecule that regulates plant metabolism and mediates defense responses against biotic and abiotic stresses. Although the cellular mechanisms by which NO is generated in plants have been intensively investigated, they still remain controversial, particularly those implicated in plant resistance to pathogens. NO can be synthesized in plants via the oxidation of -arginine into -citrulline by a nitric oxide synthase (NOS) that has no homology with the animal NOS family. In addition to -arginine, nitrite is also an important source for NO in plants. Since nitrate reductase (NR) activity is required for NO production, reduction of nitrite catalyzed by the enzyme has been considered a major NO source in plants. Recent experimental data, however, indicate that NR-defective mutant plants can synthesize NO from exogenous nitrite. Nevertheless, NR-deficient plants lack enough endogenous substrates (-arginine and nitrite) for adequate NO synthesis, resulting in an impaired hypersensitive response (HR). These findings indicate that NR activity is an important source of substrates for NO production. The main pathways for NO production from -arginine and nitrite in plants are located in mitochondria, suggesting that these organelles play a central role in NO signaling.

Plant cells exposed to anaerobic stress generate copious amounts of the gaseous free radical nitric oxide (NO). At this time, the concomitant expression of the ubiquitous class 1 plant hemoglobins establishes one component of a soluble terminal NO dioxygenase system, which yields nitrate ions via reaction of oxyhemoglobin with NO. Class 1 hemoglobin expression also enhances the cellular energy status, redox status, and NO metabolism of plant cells exposed to hypoxic stress. The ability of class 1 hemoglobins to ligate oxygen at concentrations two orders of magnitude lower than cytochrome  oxidase suggests that hemoglobin and NO may serve as components of an alternative type of respiration that is operative during conditions that impair the operation of mitochondrial terminal oxidases. We suggest that, under hypoxic conditions, NO can be formed by anaerobic reduction of nitrite by a portion of the mitochondrial electron transport chain. NADH and NADPH, accumulated due to glycolytic fermentation and lipid breakdown, contribute electrons to the process, generating a chemiosmotic potential capable of generating ATP. The overall anaerobic reaction sequence is referred to as the Hb/NO cycle.

Nitric oxide (NO), a reactive nitrogen species, serves as a signaling molecule in plants, animals, fungi, and bacteria. In spite of its potential significance, however, the unique challenges of NO research can bring confusion to investigations, primarily due to difficulties in detecting and quantifying biological NO production. To overcome such barriers, we recommend that researchers choose a combinatorial approach for monitoring NO levels, in which multiple methods having distinct detection principles are employed. After an overview of the major methodologies for NO detection, we highlight the usefulness and application limits of the fluorescence probe diaminofluorescein (DAF), which has been preferentially applied in studies of plant NO-producing systems.