The role of reactive oxygen species and oxidative stress in carbon monoxide toxicity: An in-depth analysis

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.

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NADPH Oxidase as a Therapeutic Target for Oxalate Induced Injury in Kidneys

Oxidative Medicine and Cellular Longevity ◽

10.1155/2013/462361 ◽

2013 ◽

Vol 2013 ◽

pp. 1-18 ◽

Cited By ~ 34

Author(s):

Sunil Joshi ◽

Ammon B. Peck ◽

Saeed R. Khan

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Nadph Oxidase ◽

Tissue Injury ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Reactive Oxygen ◽

Renal Tissue ◽

Oxygen Species ◽

Gene Expressions

A major role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes is to catalyze the production of superoxides and other reactive oxygen species (ROS). These ROS, in turn, play a key role as messengers in cell signal transduction and cell cycling, but when they are produced in excess they can lead to oxidative stress (OS). Oxidative stress in the kidneys is now considered a major cause of renal injury and inflammation, giving rise to a variety of pathological disorders. In this review, we discuss the putative role of oxalate in producing oxidative stress via the production of reactive oxygen species by isoforms of NADPH oxidases expressed in different cellular locations of the kidneys. Most renal cells produce ROS, and recent data indicate a direct correlation between upregulated gene expressions of NADPH oxidase, ROS, and inflammation. Renal tissue expression of multiple NADPH oxidase isoforms most likely will impact the future use of different antioxidants and NADPH oxidase inhibitors to minimize OS and renal tissue injury in hyperoxaluria-induced kidney stone disease.

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Advanced Glycation End Products and Oxidative Stress in a Hyperglycaemic Environment

10.5772/intechopen.97234 ◽

2021 ◽

Author(s):

Akio Nakamura ◽

Ritsuko Kawahrada

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Advanced Glycation End Products ◽

Reactive Oxygen ◽

Protein Glycation ◽

Oxygen Species ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products ◽

And Oxidative Stress

Protein glycation is the random, nonenzymatic reaction of sugar and protein induced by diabetes and ageing; this process is quite different from glycosylation mediated by the enzymatic reactions catalysed by glycosyltransferases. Schiff bases form advanced glycation end products (AGEs) via intermediates, such as Amadori compounds. Although these AGEs form various molecular species, only a few of their structures have been determined. AGEs bind to different AGE receptors on the cell membrane and transmit signals to the cell. Signal transduction via the receptor of AGEs produces reactive oxygen species in cells, and oxidative stress is responsible for the onset of diabetic complications. This chapter introduces the molecular mechanisms of disease onset due to oxidative stress, including reactive oxygen species, caused by AGEs generated by protein glycation in a hyperglycaemic environment.

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Flavonoids, the Family of Plant-derived Antioxidants making inroads into Novel Therapeutic Design against IR-induced Oxidative Stress in Parkinson’s Disease

Current Neuropharmacology ◽

10.2174/1570159x19666210524152817 ◽

2021 ◽

Vol 19 ◽

Author(s):

Tapan Behl ◽

Gagandeep Kaur ◽

Aayush Sehgal ◽

Gokhan Zengin ◽

Sukhbir Singh ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Ionizing Radiation ◽

Reactive Oxygen ◽

Oxygen Species ◽

Radiation Induced ◽

Novel Therapeutic

Background: Ionizing radiation from telluric sources is unceasingly an unprotected pitfall to humans. Thus, the foremost contributors to human exposure are global and medical radiations. Various pieces of evidences assembled during preceding years reveal the pertinent role of ionizing radiation-induced oxidative stress in the progression of neurodegenerative insults such as Parkinson’s disease, which have been contributing to increased proliferation and generation of reactive oxygen species. Objective: This review delineates the role of ionizing radiation-induced oxidative stress in Parkinson’s disease and proposes novel therapeutic interventions of flavonoid family offering effective management and slowing down the progression of Parkinson’s disease. Method: Published papers were searched via MEDLINE, PubMed, etc. published to date for in-depth database collection. Results: The potential of oxidative damage may harm the non-targeted cells. It can also modulate the functions of central nervous system, such as protein misfolding, mitochondria dysfunction, increased levels of oxidized lipids, and dopaminergic cell death, which accelerates the progression of Parkinson’s disease at the molecular, cellular, or tissue levels. In Parkinson’s disease, reactive oxygen species exacerbate the production of nitric oxides and superoxides by activated microglia, rendering death of dopaminergic neuronal cell through different mechanisms. Conclusion: Rising interest has extensively engrossed on the clinical trial designs based on the plant derived family of antioxidants. They are known to exert multifarious impact either way in neuroprotection via directly suppressing ionizing radiation-induced oxidative stress and reactive oxygen species production or indirectly increasing the dopamine levels and activating the glial cells.

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Underlying mechanisms of reactive oxygen species and oxidative stress photoinduced by graphene and its surface-functionalized derivatives

Environmental Science Nano ◽

10.1039/c9en01295h ◽

2020 ◽

Vol 7 (3) ◽

pp. 782-792 ◽

Cited By ~ 2

Author(s):

Hongye Yao ◽

Yang Huang ◽

Xuan Li ◽

Xuehua Li ◽

Hongbin Xie ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Functional Groups ◽

Reactive Oxygen ◽

Oxygen Species ◽

Underlying Mechanisms ◽

Transformation Processes ◽

And Oxidative Stress

Graphene can be modified by different functional groups through various transformation processes in the environment.

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Effect of Dipyridamole on the Reactive Oxygen Species and Oxidative Stress in Trabecular Meshwork Cells

Journal of the Korean Ophthalmological Society ◽

10.3341/jkos.2013.54.3.496 ◽

2013 ◽

Vol 54 (3) ◽

pp. 496

Author(s):

Keun Woo Lee ◽

Jae Woo Kim

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Trabecular Meshwork ◽

Reactive Oxygen ◽

Oxygen Species ◽

Trabecular Meshwork Cells ◽

And Oxidative Stress

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Redox Regulation and Oxidative Stress: The Particular Case of the Stallion Spermatozoa

Antioxidants ◽

10.3390/antiox8110567 ◽

2019 ◽

Vol 8 (11) ◽

pp. 567 ◽

Cited By ~ 11

Author(s):

Fernando J. Peña ◽

Cristian O’Flaherty ◽

José M. Ortiz Rodríguez ◽

Francisco E. Martín Cano ◽

Gemma L. Gaitskell-Phillips ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Redox Regulation ◽

Redox Homeostasis ◽

Reactive Oxygen ◽

Mitochondrial Activity ◽

Oxygen Species ◽

Redox Biology ◽

Major Interest ◽

And Oxidative Stress

Redox regulation and oxidative stress have become areas of major interest in spermatology. Alteration of redox homeostasis is recognized as a significant cause of male factor infertility and is behind the damage that spermatozoa experience after freezing and thawing or conservation in a liquid state. While for a long time, oxidative stress was just considered an overproduction of reactive oxygen species, nowadays it is considered as a consequence of redox deregulation. Many essential aspects of spermatozoa functionality are redox regulated, with reversible oxidation of thiols in cysteine residues of key proteins acting as an “on–off” switch controlling sperm function. However, if deregulation occurs, these residues may experience irreversible oxidation and oxidative stress, leading to malfunction and ultimately death of the spermatozoa. Stallion spermatozoa are “professional producers” of reactive oxygen species due to their intense mitochondrial activity, and thus sophisticated systems to control redox homeostasis are also characteristic of the spermatozoa in the horse. As a result, and combined with the fact that embryos can easily be collected in this species, horses are a good model for the study of redox biology in the spermatozoa and its impact on the embryo.

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Arginine Biosynthesis Modulates Pyoverdine Production and Release in Pseudomonas putida as Part of the Mechanism of Adaptation to Oxidative Stress

Journal of Bacteriology ◽

10.1128/jb.00454-19 ◽

2019 ◽

Vol 201 (22) ◽

Cited By ~ 3

Author(s):

Laura Barrientos-Moreno ◽

María Antonia Molina-Henares ◽

Marta Pastor-García ◽

María Isabel Ramos-González ◽

Manuel Espinosa-Urgel

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Amino Acid ◽

Pseudomonas Putida ◽

Reactive Oxygen ◽

Full Detail ◽

Oxygen Species ◽

Arginine Biosynthesis ◽

Content Type ◽

And Oxidative Stress

ABSTRACT Iron is essential for most life forms. Under iron-limiting conditions, many bacteria produce and release siderophores—molecules with high affinity for iron—which are then transported into the cell in their iron-bound form, allowing incorporation of the metal into a wide range of cellular processes. However, free iron can also be a source of reactive oxygen species that cause DNA, protein, and lipid damage. Not surprisingly, iron capture is finely regulated and linked to oxidative-stress responses. Here, we provide evidence indicating that in the plant-beneficial bacterium Pseudomonas putida KT2440, the amino acid l-arginine is a metabolic connector between iron capture and oxidative stress. Mutants defective in arginine biosynthesis show reduced production and release of the siderophore pyoverdine and altered expression of certain pyoverdine-related genes, resulting in higher sensitivity to iron limitation. Although the amino acid is not part of the siderophore side chain, addition of exogenous l-arginine restores pyoverdine release in the mutants, and increased pyoverdine production is observed in the presence of polyamines (agmatine and spermidine), of which arginine is a precursor. Spermidine also has a protective role against hydrogen peroxide in P. putida, whereas defects in arginine and pyoverdine synthesis result in increased production of reactive oxygen species. IMPORTANCE The results of this study show a previously unidentified connection between arginine metabolism, siderophore turnover, and oxidative stress in Pseudomonas putida. Although the precise molecular mechanisms involved have yet to be characterized in full detail, our data are consistent with a model in which arginine biosynthesis and the derived pathway leading to polyamine production function as a homeostasis mechanism that helps maintain the balance between iron uptake and oxidative-stress response systems.

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