scholarly journals Reactive Oxygen Species (ROS) Metabolism and Nitric Oxide (NO) Content in Roots and Shoots of Rice (Oryza sativa L.) Plants under Arsenic-Induced Stress

Agronomy ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1014 ◽  
Author(s):  
Ernestina Solórzano ◽  
Francisco J. Corpas ◽  
Salvador González-Gordo ◽  
José M. Palma
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Oryza Sativa ◽  
Oryza Sativa L ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Antioxidative Systems ◽  
Ros Metabolism ◽  
As Stress

Arsenic (As) is a highly toxic metalloid for all forms of life including plants. Rice is the main food source for different countries worldwide, although it can take up high amounts of As in comparison with other crops, showing toxic profiles such as decreases in plant growth and yield. The induction of oxidative stress is the main process underlying arsenic toxicity in plants, including rice, due to an alteration of the reactive oxygen species (ROS) metabolism. The aim of this work was to gain better knowledge on how the ROS metabolism and its interaction with nitric oxide (NO) operate under As stress conditions in rice plants. Thus, physiological and ROS-related biochemical parameters in roots and shoots from rice (Oryza sativa L.) were studied under 50 μM arsenate (AsV) stress, and the involvement of the main antioxidative systems and NO in the response of plants to those conditions was investigated. A decrease of 51% in root length and 27% in plant biomass was observed with 50 μM AsV treatment, as compared to control plants. The results of the activity of superoxide dismutase (SOD) isozymes, catalase, peroxidase (POD: total and isoenzymatic), and the enzymes of the ascorbate–glutathione cycle, besides the ascorbate and glutathione contents, showed that As accumulation provoked an overall significant increase of most of them, but with different profiles depending on the plant organ, either root or shoot. Among the seven identified POD isozymes, the induction of the POD-3 in shoots under As stress could help to maintain the hydrogen peroxide (H2O2) redox homeostasis and compensate the loss of the ascorbate peroxidase (APX) activity in both roots and shoots. Lipid peroxidation was slightly increased in roots and shoots from As-treated plants. The H2O2 and NO contents were enhanced in roots and shoots against arsenic stress. In spite of the increase of most antioxidative systems, a mild oxidative stress situation appears to be consolidated overall, since the growth parameters and those from the oxidative damage could not be totally counteracted. In these conditions, the higher levels of H2O2 and NO suggest that signaling events are simultaneously occurring in the whole plant.

scholarly journals The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Severe Liver ◽  
Hepatocellular Necrosis

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.

Reactive oxygen species induced by heat stress during grain filling of rice ( Oryza sativa L.) are involved in occurrence of grain chalkiness

2017 ◽  
Vol 216 ◽  
pp. 52-57 ◽  
Author(s):  
Chetphilin Suriyasak ◽  
Keisuke Harano ◽  
Koichiro Tanamachi ◽  
Kazuhiro Matsuo ◽  
Aina Tamada ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Oryza Sativa ◽  
Heat Stress ◽  
Oryza Sativa L ◽  
Reactive Oxygen ◽  
Grain Filling ◽  
Oxygen Species ◽  
Grain Chalkiness

Hygromycin B-induced cell death is partly mediated by reactive oxygen species in rice (Oryza sativa L.)

2015 ◽  
Vol 89 (6) ◽  
pp. 577-588 ◽  
Author(s):  
Hui-Min Oung ◽  
Ke-Chun Lin ◽  
Tsung-Meng Wu ◽  
Nulu Naga Prafulla Chandrika ◽  
Chwan-Yang Hong
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Oryza Sativa ◽  
Oryza Sativa L ◽  
Reactive Oxygen ◽  
Hygromycin B ◽  
Oxygen Species

Oxidative Stress and Hypertension

2021 ◽  
Vol 128 (7) ◽  
pp. 993-1020
Author(s):  
Kathy K. Griendling ◽  
Livia L. Camargo ◽  
Francisco J. Rios ◽  
Rhéure Alves-Lopes ◽  
Augusto C. Montezano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Animal Models ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Antioxidant Systems ◽  
Inflammasome Activation ◽  
Oxygen Species ◽  
Organ Systems

A link between oxidative stress and hypertension has been firmly established in multiple animal models of hypertension but remains elusive in humans. While initial studies focused on inactivation of nitric oxide by superoxide, our understanding of relevant reactive oxygen species (superoxide, hydrogen peroxide, and peroxynitrite) and how they modify complex signaling pathways to promote hypertension has expanded significantly. In this review, we summarize recent advances in delineating the primary and secondary sources of reactive oxygen species (nicotinamide adenine dinucleotide phosphate oxidases, uncoupled endothelial nitric oxide synthase, endoplasmic reticulum, and mitochondria), the posttranslational oxidative modifications they induce on protein targets important for redox signaling, their interplay with endogenous antioxidant systems, and the role of inflammasome activation and endoplasmic reticular stress in the development of hypertension. We highlight how oxidative stress in different organ systems contributes to hypertension, describe new animal models that have clarified the importance of specific proteins, and discuss clinical studies that shed light on how these processes and pathways are altered in human hypertension. Finally, we focus on the promise of redox proteomics and systems biology to help us fully understand the relationship between ROS and hypertension and their potential for designing and evaluating novel antihypertensive therapies.

scholarly journals The role of oxidative stress in alcoholic liver injury

2009 ◽  
Vol 62 (11-12) ◽  
pp. 547-553 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Alcoholic Liver Injury ◽  
Chronic Ethanol Consumption

Introduction. Oxidative stress plays an important role in pathogenesis of alcoholic liver injury. The main source of free oxygen species is cytochrome P450-dependent monooxygenase, which can be induced by ethanol. Role of cytochrome P4502E1 in ethanol-induced oxidative stress. Reactive oxygen species produced by this enzyme are more important in intracellular oxidative damage compared to species derived from activated phagocytes. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in alcohol-induced oxidative stress. Production of mitochondrial reactive oxygen species is increased, and glutathione content is decreased in chronically ethanolfed animals. Oxidative stress in mitochondria leads to mitochondrial DNA damage and has a dual effect on apoptosis. Role of Kupffer cells in alcohol-induced liver injury. Chronic ethanol consumption is associated with increased release of endotoxin from gut lumen into portal circulation. Endotoxin activates Kupffer cells, which then release proinflammatory cytokines and oxidants. Role of neutrophils in alcohol-induced liver injury. Alcoholic liver injury leads to the accumulation of neutrophils, which release reactive oxygen species and lysosomal enzymes and contribute to hepatocyte damage and necrosis. Role of nitric oxide in alcohol-induced oxidative stress. High amounts of nitric oxide contribute to the oxidative damage, mainly by generating peroxynitrites. Role of antioxidants in ethanol-induced oxidative stress. Chronic ethanol consumption is associated with reduced liver glutathione and ?-tocopherol level and with reduced superoxide dismutase, catalase and glutathione peroxidase activity. Conclusion. Oxidative stress in alcoholic liver disease is a consequence of increased production of oxidants and decreased antioxidant defense in the liver.

scholarly journals The role of nitric oxide in the maintenance of vasoactive balance

2007 ◽  
pp. S7-S16
Author(s):  
O Pecháňová ◽  
F Šimko
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Target Organ Damage ◽  
Reactive Oxygen ◽  
Decisive Role ◽  
Organ Damage ◽  
Oxygen Species ◽  
Casual Relation

Endothelial dysfunction may be considered as the interstage between risk factors and cardiovascular pathology. An imbalance between the production of vasorelaxing and vasoconstricting factors plays a decisive role in the development of hypertension, atherosclerosis and target organ damage. Except vasorelaxing and antiproliferative properties per se, nitric oxide participates in antagonizing vasoconstrictive and growth promoting effects of angiotensin II, endothelins and reactive oxygen species. Angiotensin II is a potent activator of NAD(P)H oxidase contributing to the production of reactive oxygen species. Numerous signaling pathways activated in response to angiotensin II and endothelin-1 are mediated through the increased level of oxidative stress, which seems to be in casual relation to a number of cardiovascular disturbances including hypertension. With respect to the oxidative stress, the NO molecule seems to be of ambivalent nature. On the one hand, NO is able to reduce generation of reactive oxygen species by inhibiting association of NAD(P)H oxidase subunits. On the other hand, when excessively produced, NO reacts with superoxides resulting in the formation of peroxynitrite, which is a free radical deteriorating endothelial function. The balance between vasorelaxing and vasoconstricting substances appears to be the principal issue for the physiological functioning of the vascular bed.

Detection of Reactive Oxygen Species in Oryza sativa L. (Rice)

BIO-PROTOCOL ◽  
2016 ◽  
Vol 6 (24) ◽  
Author(s):  
Navdeep Kaur ◽  
Isha Sharma ◽  
Kamal Kirat ◽  
Pratap Pati
Keyword(s):  
Reactive Oxygen Species ◽  
Oryza Sativa ◽  
Oryza Sativa L ◽  
Reactive Oxygen ◽  
Oxygen Species
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