scholarly journals Nitric oxide ameliorates stress responses in plants

2011 ◽  
Vol 57 (No. 3) ◽  
pp. 95-100 ◽  
Author(s):  
A.N. Misra ◽  
M. Misra ◽  
R. Singh

Nitric oxide (NO) is a gaseous diatomic molecule with a wide variety of physiological and pathological implications in plants. Presence of unpaired electron in its molecular orbital makes it highly reactive; it can react directly with metal complexes, radicals, DNA, proteins, lipids and other biomolecules. Nitric oxide (NO) and reactive oxygen species (ROS) are known to play essential role in a number of important plant physiological processes. This manuscript reviews the role of NO on these processes during various biotic and abiotic stresses.  

2021 ◽  
Vol 22 (17) ◽  
pp. 9656
Author(s):  
Kaiser Iqbal Wani ◽  
M. Naeem ◽  
Christian Danve M. Castroverde ◽  
Hazem M. Kalaji ◽  
Mohammed Albaqami ◽  
...  

Abiotic stressors, such as drought, heavy metals, and high salinity, are causing huge crop losses worldwide. These abiotic stressors are expected to become more extreme, less predictable, and more widespread in the near future. With the rapidly growing human population and changing global climate conditions, it is critical to prevent global crop losses to meet the increasing demand for food and other crop products. The reactive gaseous signaling molecule nitric oxide (NO) is involved in numerous plant developmental processes as well as plant responses to various abiotic stresses through its interactions with various molecules. Together, these interactions lead to the homeostasis of reactive oxygen species (ROS), proline and glutathione biosynthesis, post-translational modifications such as S-nitrosylation, and modulation of gene and protein expression. Exogenous application of various NO donors positively mitigates the negative effects of various abiotic stressors. In view of the multidimensional role of this signaling molecule, research over the past decade has investigated its potential in alleviating the deleterious effects of various abiotic stressors, particularly in ROS homeostasis. In this review, we highlight the recent molecular and physiological advances that provide insights into the functional role of NO in mediating various abiotic stress responses in plants.


2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.


2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.


2015 ◽  
Vol 66 (10) ◽  
pp. 2869-2876 ◽  
Author(s):  
Irene Serrano ◽  
María C. Romero-Puertas ◽  
Luisa M. Sandalio ◽  
Adela Olmedilla

2010 ◽  
Vol 36 (2) ◽  
pp. 239-247 ◽  
Author(s):  
Keiichi Matsubara ◽  
Yuko Matsubara ◽  
Shinji Hyodo ◽  
Tomihiro Katayama ◽  
Masaharu Ito

Peptides ◽  
2012 ◽  
Vol 37 (2) ◽  
pp. 314-319 ◽  
Author(s):  
Mahdieh Faghihi ◽  
Ali Mohammad Alizadeh ◽  
Vahid Khori ◽  
Mostafa Latifpour ◽  
Saeed Khodayari

Author(s):  
Isabel Manrique-Gil ◽  
Inmaculada Sánchez-Vicente ◽  
Isabel Torres-Quezada ◽  
Oscar Lorenzo

Abstract Plants are aerobic organisms that have evolved to maintain specific requirements for oxygen (O2), leading to a correct respiratory energy supply during growth and development. There are certain plant developmental cues and biotic or abiotic stress responses where O2 is scarce. This O2 deprivation known as hypoxia may occur in hypoxic niches of plant-specific tissues and during adverse environmental cues such as pathogen attack and flooding. In general, plants respond to hypoxia through a complex reprogramming of their molecular activities with the aim of reducing the impact of stress on their physiological and cellular homeostasis. This review focuses on the fine-tuned regulation of hypoxia triggered by a network of gaseous compounds that includes O2, ethylene, and nitric oxide. In view of recent scientific advances, we summarize the molecular mechanisms mediated by phytoglobins and by the N-degron proteolytic pathway, focusing on embryogenesis, seed imbibition, and germination, and also specific structures, most notably root apical and shoot apical meristems. In addition, those biotic and abiotic stresses that comprise hypoxia are also highlighted.


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