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Nitric oxide and antioxidant properties

Nitric oxide and antioxidant properties

Recently, 8-nitro-cGMP was uncovered as a down-stream Diabetes management system of ABA, NO, propefties ROS in inducing oxode closure at daytime, whereas cGMP regulated stomatal opening at night Joudoi et al. Hypothetical model on the dynamic interaction between NO, ROS and the antioxidant system under stress conditions. and Gutteridge, J. Nitric oxide and antioxidant properties

Nitric oxide and antioxidant properties -

Suppression of the pathogen-induced H 2 O 2 burst by the NADPH oxidase inhibitor diphenylene iodonium DPI prevented cell death whereas low millimolar concentrations of exogenous H 2 O 2 triggered HR-PCD in a calcium-dependent manner Levine et al.

Later, researchers of the same group demonstrated that NO was another essential messenger in cell death execution Delledonne et al. Application of a NO scavenger and a NOS activity inhibitor both reduced HR-PCD of soybean suspension cells infected with avirulent bacterial pathogens. Importantly, SNP triggered cell death most efficiently in conjunction with ROS but not in the presence of DPI or CAT.

ROS donors in turn efficiently killed soybean cells only if applied together with SNP Delledonne et al. Comparable results were obtained with tobacco BY-2 cells.

Therefore, it was postulated that NO and ROS cooperate in cell death signaling Figure 2. Recent studies have begun to unravel the underlying modes of interactions between NO, ROS and the antioxidant system during PCD.

thaliana plants challenged by avirulent Pseudomonas syringae Gaupels et al. However, contrary to mammalian cells this RNS does not kill plant cells Delledonne et al.

If this is a significant process in vivo remains to be proven. This particular ROS acts as an inducer of NO synthesis in tobacco cells De Pinto et al. For instance, rice knock-out mutants defective in a CAT-coding gene showed increased H 2 O 2 levels, nitrate reductase-dependent accumulation of NO and spontaneous leaf cell death Lin et al.

Application of the NO scavenger PTIO mitigated the cell death phenotype. The importance of a down-regulation of ROS detoxifying enzymes during PCD was further corroborated by the finding that overexpression of thylakoidal APX led to a higher resistance against SNP induced cell death Murgia et al.

thaliana WT plants 5mM SNP triggered H 2 O 2 accumulation and cell death, which was both reduced in the transgenic line probably because H 2 O 2 was degraded by the elevated APX activity in these plants. The antioxidant enzymes CAT and APX control H 2 O 2 levels under mild stress conditions.

Severe cadmium stress triggered NO as well as H 2 O 2 accumulation and senescence-like PCD of A. thaliana suspension cultured cells De Michele et al. However, co-treatment with the NOS inhibitor L-NMMA prevented the NO-dependent inhibition of CAT and APX, which in turn reduced H 2 O 2 levels and increased cell viability under cadmium stress.

Mechanical wounding provokes cell damage, which could serve as a point of entry into the plant e. To avoid this, PCD is triggered in intact cells nearby the damaged cells for sealing the wound site. In wounded leaves of Pelargonium peltatum NO accumulation was restricted to the site of injury Arasimowicz et al.

Treatment with cPTIO confirmed that NO inhibited APX and CAT activity thereby temporarily enhancing the H 2 O 2 content at the edge of the wound. Pre-treatment of leaves with NO donors before wounding prevented the H 2 O 2 burst and reduced necrotic cell death in sweet potato Lin et al.

The exact mechanism of NO action was not determined but available data suggest that APX, GR, MDHAR and thioredoxin are S-nitrosylated during PCD, which could affect their activity Murgia et al. Inhibition of GR and MDHAR would also impact on the redox status of the glutathione and ascorbate pools.

It should be considered that enzymatic activity can also be influenced by ROS-dependent modifications, which was proposed for oxidation-triggered inhibition of APX Figure 2 De Pinto et al.

The latter enzyme was also suppressed in gene expression during PCD De Pinto et al. The role of NO in incompatible interactions between A. thaliana and avirulent Pseudomonas syringae was investigated using transgenic plant lines expressing a bacterial NO dioxygenase NOD, flavohemoglobin Zeier et al.

NOD expression attenuated the pathogen-induced NO accumulation. As a consequence the H 2 O 2 burst was diminished and transgenic plants developed less HR-PCD and were delayed in SA-dependent PR1 expression. These results support again the hypothesis that high levels of NO amplify redox signaling during PCD by inhibiting the plant antioxidant machinery Zeier et al.

NO and H 2 O 2 might mutually enhance each other's accumulation by positive feed-back regulation. To this end, NO and ROS producing enzymes as well as elements of the antioxidant system must be regulated in a highly coordinate fashion for initiation of PCD.

The exact signaling pathways remain to be deciphered in future studies. However, the plant must also constrain stress signaling by NO, ROS and the antioxidant system for avoiding excessive damage by runaway cell death.

Therefore, it is worth mentioning that both ROS as well as NO were found to induce genes involved in cell protection such as a gene coding for glutathione S-transferase Levine et al. Yun and colleagues Yun et al. thaliana challenged by avirulent bacteria.

The authors proposed a model, in which the early burst of ROS and NO initiates HR-PCD but at later stages of the defence response the SNO levels exceed a certain threshold and subsequently the AtRBOHD is inactivated by S-nitrosylation at Cys , which terminates the HR.

In contrast to R gene-mediated resistance against avirulent pathogens, bacterial lipopolysaccharides LPS elicit basal pathogen resistance without onset of HR-PCD.

LPS-induced NO synthesis by an arginine-dependent enzymatic source even protected plant cells against oxidative stress and cell death by enhancing the activities of CAT, SOD, and POD.

The changed cellular redox status contributed to the regulation of NPR1-dependent expression of defence genes Sun et al. In sum, NO can either act as an inducer or suppressor of plant PCD dependent on its local cellular levels and its tightly controlled interaction with ROS and elements of the antioxidant system Figure 2.

ROS and NO are increasingly recognized signaling molecules in plant physiology. While research on ROS has a long history NO came into focus only 15 years ago. In the present paper we reviewed recent literature dealing with the interaction between ROS, NO and the antioxidant system during stress defence.

As one interesting outcome we found that exposure of plants to unfavorable conditions inevitably induced ROS but not necessarily NO accumulation. In contrast, NO is rather a highly specialized second messenger, which modifies ROS signaling or acts independently of ROS.

Significantly, ROS and NO bursts are often triggered simultaneously—sometimes even in the same cellular compartment. Particularly chloroplasts and peroxisomes are hotspots of NO-ROS interactions. More indirect interactions include induction of NO synthesis by H 2 O 2 and accumulation of ROS due to inhibition of antioxidant enzymes by NO-dependent protein modifications.

Therefore, plants have developed efficient measures for controlling NO levels by GSNOR, hemoglobins and other RNS scavenging enzymes.

This review was also aimed at investigating the extreme versatility of possible reactions between NO, ROS and the antioxidant system. More basic research is urgently needed for defining chemical reactions and their products actually occurring in planta.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Mechanisms of the antioxidant effects of nitric oxide. Overview Fingerprint. Abstract The Janus face of nitric oxide NO has prompted a debate as to whether NO plays a deleterious or protective role in tissue injury. ASJC Scopus subject areas Biochemistry Physiology Molecular Biology Clinical Biochemistry Cell Biology.

Access to Document Link to publication in Scopus. Link to the citations in Scopus. Fingerprint Dive into the research topics of 'Mechanisms of the antioxidant effects of nitric oxide'.

Together they form a unique fingerprint. View full fingerprint. Cite this APA Standard Harvard Vancouver Author BIBTEX RIS Wink, D. Antioxidants and Redox Signaling , 3 2 , et al. In: Antioxidants and Redox Signaling , Vol. Wink DA, Miranda KM, Espey MG, Pluta RM , Hewett SJ , Colton C et al.

Antioxidants and Redox Signaling. doi: Wink, David A. In: Antioxidants and Redox Signaling. TY - JOUR T1 - Mechanisms of the antioxidant effects of nitric oxide AU - Wink, David A. AU - Miranda, Katrina M.

David Antioxidannt. Wink, Katrina M. Miranda, Michael G. Espey, Ryzard M. Pluta, Sandra J. Gymnastics diet essentials for athletes Diabetes management system reacts preferentially with other free radicals. Reaction of nitric oxide Nitdic oxygen yields nitrogen dioxide, a potent oxidant. However, this propdrties may antioxidannt too slow to be relevant in vivo. Diabetes management system of Nitric oxide and antioxidant properties oxide with superoxide occurs extremely rapidly and generates peroxynitrite. This latter molecule undergoes many deleterious oxidative reactions with biological molecules such as amino acids, sugars and lipids. In an analagous reaction nitric oxide may also react with peroxyl radicals, such as lipid peroxyl radicals, and inhibit free radical chain reactions such as lipid peroxidation. This chapter discusses experimental sources of nitric oxide and peroxyntirite and the potential pro-oxidant and antioxidant effects of nitric oxide in biological systems.


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