scholarly journals Coordination of frontline defense mechanisms under severe oxidative stress

2010 ◽  
Vol 6 (1) ◽  
pp. 393 ◽  
Author(s):  
Amardeep Kaur ◽  
Phu T Van ◽  
Courtney R Busch ◽  
Courtney K Robinson ◽  
Min Pan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms

scholarly journals Pathomechanisms of Oxidative Stress in Inflammatory Bowel Disease and Potential Antioxidant Therapies

2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Tian Tian ◽  
Ziling Wang ◽  
Jinhua Zhang
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Defense Mechanisms ◽  
Gastrointestinal Disease ◽  
Mucosal Immune Response ◽  
Stress Signaling ◽  
Substantial Progress ◽  
Inflammatory Bowel ◽  
Underlying Mechanisms

Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease whose incidence has risen worldwide in recent years. Accumulating evidence shows that oxidative stress plays an essential role in the pathogenesis and progression of IBD. This review highlights the generation of reactive oxygen species (ROS) and antioxidant defense mechanisms in the gastrointestinal (GI) tract, the involvement of oxidative stress signaling in the initiation and progression of IBD and its relationships with genetic susceptibility and the mucosal immune response. In addition, potential therapeutic strategies for IBD that target oxidative stress signaling are reviewed and discussed. Though substantial progress has been made in understanding the role of oxidative stress in IBD in humans and experimental animals, the underlying mechanisms are still not well defined. Thus, further studies are needed to validate how oxidative stress signaling is involved in and contributes to the development of IBD.

Insights into the Relation between Oxidative Stress and Malaria: A Mechanistic and Therapeutic Approach

2021 ◽  
Vol 11 ◽  
Author(s):  
Abhijit Sarkar ◽  
Swarnendu Basak ◽  
Sumit Ghosh ◽  
Sushweta Mahalanobish ◽  
Parames C. Sil
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Preventive Measures ◽  
Host Immunity ◽  
Malarial Parasite ◽  
Malarial Infection ◽  
Parasitic Load ◽  
Therapeutic Mechanisms ◽  
Antioxidant Effects ◽  
Oxidative Insult

The mortality rate due to malaria has increased tremendously in the last decade. Even though the causative agent of this disease is known, the preventive measures are not potent enough to control the spread of this disease. Malarial infection involves a strong interrelationship between oxidative stress and pathogenesis. This review addresses the various oxidative stress-related mechanisms associated with vector defense, host immunity, plasmodial pathogenesis, and corresponding therapeutic strategies. The mechanisms involving host and vector defense show both similarity and contradiction to the processes involving plasmodial pathogenesis under different circumstances. Therefore, corresponding ameliorative peculiarities are observed in the therapeutic mechanisms adopted by the anti-malarial drugs. The malarial parasite augments oxidative stress to weaken the host and exerts antioxidant effects against host defense mechanisms. However, the anti-malarial drugs induce oxidative insult to reduce parasitic load and exert antioxidant effects against parasite infection-induced oxidative stress in host. Thus, the anti-malarial drugs exhibit antioxidant activity in hosts and/or pro-oxidant activity in parasites.

scholarly journals Protein carbonyl group content in patients affected by familiar chronic nail candidiasis

2003 ◽  
Vol 12 (4) ◽  
pp. 247-249 ◽  
Author(s):  
S. Gangemi ◽  
A. Saija ◽  
A. Tomaino ◽  
F. Cimino ◽  
R. A. Merendino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Protein Carbonyl ◽  
Intercellular Adhesion Molecule ◽  
Carbonyl Groups ◽  
Intercellular Adhesion Molecule 1 ◽  
Protein Carbonyl Groups ◽  
Halide System ◽  
Reactive Nitrogen Intermediates ◽  
Hands And Feet

Familiar chronic nail candidiasis (FCNC) is a rare disorder characterized by early-onset infections caused by different species of Candida, restricted to the nail of the hands and feet, and associated with a low serum concentration of intercellular adhesion molecule 1. Host defense mechanisms against candidiasis require the cooperation of many immune cells through several candidacidal mechanisms, including oxygen-dependent killing mechanisms, mediated by a superoxide anion radical myeloperoxidase-H2O2-halide system, and reactive nitrogen intermediates. We analyzed protein carbonyl groups (considered a useful marker of oxidative stress) in the serum of patients belonging to a five-generation Italian family with an isolated form of FCNC.Serum protein carbonyl groups in FCNC patients were significantly lower than those measured in healthy donors.Also, if this hypothesis is merely speculative, we could suggest that the decreased circulating level of protein carbonyl groups in these patients is not a marker of a lower oxidative stress condition, but might be linked to a lower protease activity.

scholarly journals Macrophage Autophagy and Oxidative Stress: An Ultrastructural and Immunoelectron Microscopical Study

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Ida Perrotta ◽  
Valentina Carito ◽  
Emilio Russo ◽  
Sandro Tripepi ◽  
Saveria Aquila ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Defense Mechanisms ◽  
Ultrastructural Localization ◽  
Microscopical Study ◽  
Beclin 1 ◽  
Cell Organelles ◽  
A Cell ◽  
First Time

The word autophagy broadly refers to the cellular catabolic processes that lead to the removal of damaged cytosolic proteins or cell organelles through lysosomes. Although autophagy is often observed during programmed cell death, it may also serve as a cell survival mechanism. Accumulation of reactive oxygen species within tissues and cells induces various defense mechanisms or programmed cell death. It has been shown that, besides inducing apoptosis, oxidative stress can also induce autophagy. To date, however, the regulation of autophagy in response to oxidative stress remains largely elusive and poorly understood. Therefore, the present study was designed to examine the ratio between oxidative stress and autophagy in macrophages after oxidant exposure (AAPH) and to investigate the ultrastructural localization of beclin-1, a protein essential for autophagy, under basal and stressful conditions. Our data provide evidence that oxidative stress induces autophagy in macrophages. We demonstrate, for the first time by immunoelectron microscopy, the subcellular localization of beclin-1 in autophagic cells.

The role of corneal crystallins in the cellular defense mechanisms against oxidative stress

2008 ◽  
Vol 19 (2) ◽  
pp. 100-112 ◽  
Author(s):  
Natalie Lassen ◽  
William J. Black ◽  
Tia Estey ◽  
Vasilis Vasiliou
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Cellular Defense

scholarly journals Mineral Micronutrients in Asthma

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4001
Author(s):  
Dominika Zajac
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Air Pollution ◽  
Defense Mechanisms ◽  
Redox Status ◽  
Chronic Inflammatory Disease ◽  
Modern World ◽  
Medical Issues ◽  
Persistent Inflammation ◽  
The Impact

Asthma represents one of the most common medical issues in the modern world. It is a chronic inflammatory disease characterized by persistent inflammation of the airways and disturbances in redox status, leading to hyperresponsiveness of bronchi and airway obstruction. Apart from classical risk factors such as air pollution, family history, allergies, or obesity, disturbances of the levels of micronutrients lead to impairments in the defense mechanisms of the affected organism against oxidative stress and proinflammatory stimuli. In the present review, the impact of micronutrients on the prevalence, severity, and possible risk factors of asthma is discussed. Although the influence of classical micronutrients such as selenium, copper, or zinc are well known, the effects of those such as iodine or manganese are only rarely mentioned. As a consequence, the aim of this paper is to demonstrate how disturbances in the levels of micronutrients and their supplementation might affect the course of asthma.

scholarly journals The investigation into neurotoxicity mechanisms of Nonylphenol: A narrative review

2020 ◽  
Vol 18 ◽  
Author(s):  
Mandana Lotfi ◽  
Amir Hosseyn Hasanpour ◽  
Ali Akbar Moghadamnia ◽  
Sohrab Kazemi
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Health Hazard ◽  
Learning Disorders ◽  
Inflammatory Factors ◽  
Postnatal Exposure ◽  
Memory And Learning ◽  
Nonylphenol Ethoxylate ◽  
Intracellular Calcium Ion ◽  
The Brain

Background: Nonylphenol (NP), as a chemical compound that widely used in industry, is the result of the nonylphenol ethoxylate decomposition and it is known as an estrogen-like compound. Numerous studies and researches have shown that it has many destructive functions of various organs such as the brain. This toxicant causes oxidative stress in the cortex and hippocampus cells, which are two essential regions to preserve memory and learning in the brain. Methods: This review examines recent findings to better understand the mechanisms of NP neurotoxicity. We used Scopus, Google Scholar and PubMed databases to find articles with focus on the destructive effects of NP on the oxidative stress pathway and its defense mechanisms. Results: NP has potential human health hazard associated with gestational, peri- and postnatal exposure. NP can disrupt brain homeostasis in different ways, such as activation of inflammatory factors in brain especially in hippocampus and cortex, disruption of the cell cycle, changes in neuron, dendrites and synapses morphology, disruption of extra and intracellular calcium ion balance and also memory and learning disorders

scholarly journals Hyperbaric Oxygen Treatment: Effects on Mitochondrial Function and Oxidative Stress

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1827
Author(s):  
Nofar Schottlender ◽  
Irit Gottfried ◽  
Uri Ashery
Keyword(s):  
Oxidative Stress ◽  
Hyperbaric Oxygen ◽  
Mitochondrial Function ◽  
Defense Mechanisms ◽  
Term Treatment ◽  
Mitochondrial Activity ◽  
Hyperbaric Oxygen Treatment ◽  
Oxygen Treatment ◽  
Long Term Treatment ◽  
And Oxidative Stress

Hyperbaric oxygen treatment (HBOT)—the administration of 100% oxygen at atmospheric pressure (ATA) greater than 1 ATA—increases the proportion of dissolved oxygen in the blood five- to twenty-fold. This increase in accessible oxygen places the mitochondrion—the organelle that consumes most of the oxygen that we breathe—at the epicenter of HBOT’s effects. As the mitochondrion is also a major site for the production of reactive oxygen species (ROS), it is possible that HBOT will increase also oxidative stress. Depending on the conditions of the HBO treatment (duration, pressure, umber of treatments), short-term treatments have been shown to have deleterious effects on both mitochondrial activity and production of ROS. Long-term treatment, on the other hand, improves mitochondrial activity and leads to a decrease in ROS levels, partially due to the effects of HBOT, which increases antioxidant defense mechanisms. Many diseases and conditions are characterized by mitochondrial dysfunction and imbalance between ROS and antioxidant scavengers, suggesting potential therapeutic intervention for HBOT. In the present review, we will present current views on the effects of HBOT on mitochondrial function and oxidative stress, the interplay between them and the implications for several diseases.

Antioxidant defenses and metabolic depression in a pulmonate land snail

1995 ◽  
Vol 268 (6) ◽  
pp. R1386-R1393 ◽  
Author(s):  
M. Hermes-Lima ◽  
K. B. Storey
Keyword(s):  
Oxidative Stress ◽  
Glutathione Peroxidase ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Thiobarbituric Acid ◽  
Land Snail ◽  
Land Snails ◽  
Antioxidant Defenses ◽  
Glutathione S Transferase ◽  
Hypometabolic State

During arousal from estivation oxygen consumption by land snails (Otala lactea) increases severalfold. To determine whether snails prepared for an accompanying rise in the rates of oxyradical generation by altering their antioxidant defense mechanisms, changes in the activities of antioxidant enzymes and lipid peroxidation products were quantified in foot and hepatopancreas of control, 30-day estivating, and aroused snails. Compared with controls, estivating O. lactea showed significant increases in the activities of foot muscle superoxide dismutase (SOD) (increasing by 56-67%), catalase (51-72%), and glutathione S-transferase (79-108%), whereas, in hepatopancreas, SOD (57-78%) and glutathione peroxidase (93-144%) increased. Within 40 min after arousal began, hepatopancreas glutathione peroxidase activity had returned to control values, but SOD showed a further 70% increase in activity but then returned to control levels by 80 min. Estivation had no effect on total glutathione (GSH + 2 GSSG) concentrations in tissues, but GSSG content had increased about twofold in both organs of 30-day dormant snails. Lipid peoxidation (quantified as thiobarbituric acid reactive substances) was significantly enhanced at the onset of arousal from dormancy, indicating that oxidative stress and tissue damage occurred at this time. The data suggest that antioxidant defenses in snail organs are increased while snails are in the hypometabolic state as a preparation for oxidative stress during arousal.

scholarly journals Oxidative Stress and Nucleic Acid Oxidation in Patients with Chronic Kidney Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Chih-Chien Sung ◽  
Yu-Chuan Hsu ◽  
Chun-Chi Chen ◽  
Yuh-Feng Lin ◽  
Chia-Chao Wu
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Nucleic Acid ◽  
Kidney Disease ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Enzyme Inhibitor ◽  
Alpha Tocopherol ◽  
Acid Oxidation ◽  
Clinical Biomarkers

Patients with chronic kidney disease (CKD) have high cardiovascular mortality and morbidity and a high risk for developing malignancy. Excessive oxidative stress is thought to play a major role in elevating these risks by increasing oxidative nucleic acid damage. Oxidative stress results from an imbalance between reactive oxygen/nitrogen species (RONS) production and antioxidant defense mechanisms and can cause vascular and tissue injuries as well as nucleic acid damage in CKD patients. The increased production of RONS, impaired nonenzymatic or enzymatic antioxidant defense mechanisms, and other risk factors including gene polymorphisms, uremic toxins (indoxyl sulfate), deficiency of arylesterase/paraoxonase, hyperhomocysteinemia, dialysis-associated membrane bioincompatibility, and endotoxin in patients with CKD can inhibit normal cell function by damaging cell lipids, arachidonic acid derivatives, carbohydrates, proteins, amino acids, and nucleic acids. Several clinical biomarkers and techniques have been used to detect the antioxidant status and oxidative stress/oxidative nucleic acid damage associated with long-term complications such as inflammation, atherosclerosis, amyloidosis, and malignancy in CKD patients. Antioxidant therapies have been studied to reduce the oxidative stress and nucleic acid oxidation in patients with CKD, including alpha-tocopherol, N-acetylcysteine, ascorbic acid, glutathione, folic acid, bardoxolone methyl, angiotensin-converting enzyme inhibitor, and providing better dialysis strategies. This paper provides an overview of radical production, antioxidant defence, pathogenesis and biomarkers of oxidative stress in patients with CKD, and possible antioxidant therapies.

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