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      Generation mechanism of hydroxyl radical species and its lifetime prediction during the plasma-initiated ultraviolet (UV) photolysis

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          Abstract

          Through this work, we have elucidated the mechanism of hydroxyl radicals (OH ) generation and its life time measurements in biosolution. We observed that plasma-initiated ultraviolet (UV) photolysis were responsible for the continues generation of OH species, that resulted in OH to be major reactive species (RS) in the solution. The density and lifetime of OH species acted inversely proportional to each other with increasing depth inside the solution. The cause of increased lifetime of OH inside the solution is predicted using theoretical and semiempirical calculations. Further, to predict the mechanism of conversion of hydroxide ion (OH ) to OH or H 2O 2 (hydrogen peroxide) and electron, we determined the current inside the solution of different pH. Additionally, we have investigated the critical criterion for OH interaction on cancer cell inducing apoptosis under effective OH exposure time. These studies are innovative in the field of plasma chemistry and medicine.

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          Nitric oxide functions as a signal in plant disease resistance.

          Recognition of an avirulent pathogen triggers the rapid production of the reactive oxygen intermediates superoxide (O2-) and hydrogen peroxide (H2O2). This oxidative burst drives crosslinking of the cell wall, induces several plant genes involved in cellular protection and defence, and is necessary for the initiation of host cell death in the hypersensitive disease-resistance response. However, this burst is not enough to support a strong disease-resistance response. Here we show that nitric oxide, which acts as a signal in the immune, nervous and vascular systems, potentiates the induction of hypersensitive cell death in soybean cells by reactive oxygen intermediates and functions independently of such intermediates to induce genes for the synthesis of protective natural products. Moreover, inhibitors of nitric oxide synthesis compromise the hypersensitive disease-resistance response of Arabidopsis leaves to Pseudomonas syringae, promoting disease and bacterial growth. We conclude that nitric oxide plays a key role in disease resistance in plants.
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            The role of reactive oxygen and antioxidant species in periodontal tissue destruction.

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              Identification of a plant nitric oxide synthase gene involved in hormonal signaling.

              Nitric oxide (NO) serves as a signal in plants. An Arabidopsis mutant (Atnos1) was identified that had impaired NO production, organ growth, and abscisic acid-induced stomatal movements. Expression of AtNOS1 with a viral promoter in Atnos1 mutant plants resulted in overproduction of NO. Purified AtNOS1 protein used the substrates arginine and nicotinamide adenine dinucleotide phosphate and was activated by Ca2+ and calmodulin-like mammalian endothelial nitric oxide synthase and neuronal nitric oxide synthase, yet it is a distinct enzyme with no sequence similarities to any mammalian isoform. Thus, AtNOS1 encodes a distinct nitric oxide synthase that regulates growth and hormonal signaling in plants.
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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                20 March 2015
                2015
                : 5
                : 9332
                Affiliations
                [1 ]Plasma Bioscience Research Center, Kwangwoon University , Seoul, Korea
                [2 ]Yonsei University , Seoul, Korea
                [3 ]Drexel Plasma Institute, Drexel University , PA, USA
                Author notes
                Article
                srep09332
                10.1038/srep09332
                4367430
                25790968
                f716480f-0769-419a-bf57-0e81de9466b7
                Copyright © 2015, Macmillan Publishers Limited. All rights reserved

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 17 October 2014
                : 16 February 2015
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