scholarly journals Oxidative Stress in the Brain: Basic Concepts and Treatment Strategies in Stroke

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1886
Author(s):  
Matyas Jelinek ◽  
Michal Jurajda ◽  
Kamil Duris
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Treatment Strategies ◽  
Ischemic Damage ◽  
Physiological Conditions ◽  
Pathological Conditions ◽  
Basic Concepts ◽  
Antioxidant Mechanisms ◽  
The Brain ◽  
High Metabolic Activity

The production of free radicals is inevitably associated with metabolism and other enzymatic processes. Under physiological conditions, however, free radicals are effectively eliminated by numerous antioxidant mechanisms. Oxidative stress occurs due to an imbalance between the production and elimination of free radicals under pathological conditions. Oxidative stress is also associated with ageing. The brain is prone to oxidative damage because of its high metabolic activity and high vulnerability to ischemic damage. Oxidative stress, thus, plays a major role in the pathophysiology of both acute and chronic pathologies in the brain, such as stroke, traumatic brain injury or neurodegenerative diseases. The goal of this article is to summarize the basic concepts of oxidative stress and its significance in brain pathologies, as well as to discuss treatment strategies for dealing with oxidative stress in stroke.

scholarly journals Antioxidants: a brief review

2018 ◽  
Vol 8 (6-s) ◽  
pp. 373-376
Author(s):  
Rekha Bisht
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Free Radical ◽  
Physiological Function ◽  
Butylated Hydroxytoluene ◽  
Oxygen Species ◽  
Synthetic Antioxidants ◽  
Pathological Conditions ◽  
External Sources ◽  
Free Radical Chemistry

The field of free radical chemistry has gained a great deal of attention in recent years. Free radicals reactive oxygen species generated by our body by various endogenous systems leads to various pathological conditions. A balance between free radicals and antioxidants is prerequisite for proper physiological function. Oxidative stress caused by generation of free radicals adversely alters lipids, proteins, and DNA and provokes a number of human ailments. Oxidative stress can be managed by using external sources of antioxidants. Synthetic antioxidants such as butylated hydroxytoluene and butylated hydroxyanisole have recently been reported to be harmful for human health. Thus, the search for effective, nontoxic natural compounds with antioxidant activity has been escalated in recent years. The present review provides a brief overview on antioxidants and natural sources of antioxidants in the management of human diseases. Keywords: free radical, Oxidative stress, antioxidants,

scholarly journals The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
M. Jelinek ◽  
M. Jurajda ◽  
K. Duris
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Molecular Mechanisms ◽  
Early Brain Injury ◽  
Pathophysiological Mechanisms ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Antioxidant Mechanisms

This review focuses on the problem of oxidative stress in early brain injury (EBI) after spontaneous subarachnoid hemorrhage (SAH). EBI involves complex pathophysiological mechanisms, including oxidative stress. In the first section, we describe the main sources of free radicals in EBI. There are several sources of excessive generation of free radicals from mitochondrial free radicals’ generation and endoplasmic reticulum stress, to hemoglobin and enzymatic free radicals’ generation. The second part focuses on the disruption of antioxidant mechanisms in EBI. The third section describes some newly found molecular mechanisms and pathway involved in oxidative stress after EBI. The last section is dedicated to the pathophysiological mechanisms through which free radicals mediate early brain injury.

Vitamin C and Thiobarbituric Acid Reactive Substances (TBARS) in Psoriasis Vulgaris Related to Psoriasis Area Severity Index (PASI)

2017 ◽  
Vol 68 (1) ◽  
pp. 43-47 ◽  
Author(s):  
Mircea Tampa ◽  
Ilinca Nicolae ◽  
Corina Daniela Ene ◽  
Isabela Sarbu ◽  
Clara Matei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Vitamin C ◽  
Psoriasis Vulgaris ◽  
Thiobarbituric Acid ◽  
Severity Index ◽  
Thiobarbituric Acid Reactive Substances ◽  
Psoriasis Area Severity Index ◽  
Pathogenic Potential ◽  
Antioxidant Mechanisms

Oxidative stress is caused by an imbalance between the production of pro-oxidants and the capacity of a biological system of rapid detoxification of free radicals. In this paper the level of pro-oxidants and antioxidants was quantified in patients with psoriasis vulgaris. The results of this study show that the level of oxygen reactive species dramatically increases and the physiologic antioxidant mechanisms are inefficient in patients with psoriasis vulgaris. These findings re-confirm that oxidative stress has a destructive and pathogenic potential in psoriasis.

scholarly journals Reactive Oxygen Species and the Cardiovascular System

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Yannick J. H. J. Taverne ◽  
Ad J. J. C. Bogers ◽  
Dirk J. Duncker ◽  
Daphne Merkus
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Oxygen Consumption ◽  
Free Radicals ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cellular Homeostasis ◽  
Cardiovascular Pathology ◽  
Pathological Conditions ◽  
By Products

Ever since the discovery of free radicals, many hypotheses on the deleterious actions of reactive oxygen species (ROS) have been proposed. However, increasing evidence advocates the necessity of ROS for cellular homeostasis. ROS are generated as inherent by-products of aerobic metabolism and are tightly controlled by antioxidants. Conversely, when produced in excess or when antioxidants are depleted, ROS can inflict damage to lipids, proteins, and DNA. Such a state of oxidative stress is associated with many pathological conditions and closely correlated to oxygen consumption. Although the deleterious effects of ROS can potentially be reduced by restoring the imbalance between production and clearance of ROS through administration of antioxidants (AOs), the dosage and type of AOs should be tailored to the location and nature of oxidative stress. This paper describes several pathways of ROS signaling in cellular homeostasis. Further, we review the function of ROS in cardiovascular pathology and the effects of AOs on cardiovascular outcomes with emphasis on the so-called oxidative paradox.

scholarly journals Molecules and Mechanisms to Overcome Oxidative Stress Inducing Cardiovascular Disease in Cancer Patients

Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 105
Author(s):  
Francesco Sabbatino ◽  
Valeria Conti ◽  
Luigi Liguori ◽  
Giovanna Polcaro ◽  
Graziamaria Corbi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Ros Production ◽  
Oxygen Species ◽  
Physiological Conditions ◽  
Cellular Processes ◽  
Pathological Conditions ◽  
Detoxification Systems ◽  
Cancer Diseases

Reactive oxygen species (ROS) are molecules involved in signal transduction pathways with both beneficial and detrimental effects on human cells. ROS are generated by many cellular processes including mitochondrial respiration, metabolism and enzymatic activities. In physiological conditions, ROS levels are well-balanced by antioxidative detoxification systems. In contrast, in pathological conditions such as cardiovascular, neurological and cancer diseases, ROS production exceeds the antioxidative detoxification capacity of cells, leading to cellular damages and death. In this review, we will first describe the biology and mechanisms of ROS mediated oxidative stress in cardiovascular disease. Second, we will review the role of oxidative stress mediated by oncological treatments in inducing cardiovascular disease. Lastly, we will discuss the strategies that potentially counteract the oxidative stress in order to fight the onset and progression of cardiovascular disease, including that induced by oncological treatments.

scholarly journals Reactive Oxygen Species in Neurodegenerative Diseases: Implications in Pathogenesis and Treatment Strategies

2021 ◽  
Author(s):  
Johnson Olaleye Oladele ◽  
Adenike T. Oladiji ◽  
Oluwaseun Titilope Oladele ◽  
Oyedotun M. Oyeleke
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Protein Misfolding ◽  
Critical Role ◽  
Treatment Strategies ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
The Brain

Neurodegenerative diseases are debilitating disorders which compromise motor or cognitive functions and are rapidly becoming a global communal disorder with over 46.8 million people suffering dementia worldwide. Aetiological studies have showed that people who are exposed to agricultural, occupational and environmental toxic chemicals that can interfere and degenerate dopaminergic neurons are prone to developing neurodegenerative diseases such as Parkinson Disease. The complex pathogenesis of the neurodegenerative diseases remains largely unknown; however, mounting evidence suggests that oxidative stress, neuroinflammation, protein misfolding, and apoptosis are the hallmarks of the diseases. Reactive oxygen species (ROS) are chemically reactive molecules that have been implicated in the pathogenesis of neurodegenerative diseases. ROS play a critical role as high levels of oxidative stress are commonly observed in the brain of patients with neurodegenerative disorders. This chapter focus on the sources of ROS in the brain, its involvement in the pathogenesis of neurodegenerative diseases and possible ways to mitigate its damaging effects in the affected brain.

scholarly journals Similarities and Differences in the Pattern of Tau Hyperphosphorylation in Physiological and Pathological Conditions: Impacts on the Elaboration of Therapies to Prevent Tau Pathology

2021 ◽  
Vol 11 ◽  
Author(s):  
Antoine Duquette ◽  
Camille Pernègre ◽  
Ariane Veilleux Carpentier ◽  
Nicole Leclerc
Keyword(s):  
Protein A ◽  
Hyperphosphorylated Tau ◽  
Tau Hyperphosphorylation ◽  
Therapeutic Approaches ◽  
Tau Pathology ◽  
Physiological Conditions ◽  
The Third ◽  
Pathological Conditions ◽  
The Brain

Tau protein, a neuronal microtubule-associated protein, becomes hyperphosphorylated in several neurodegenerative diseases called tauopathies. Hyperphosphorylation of tau is correlated to its redistribution from the axon to the somato-dendritic compartment at early stages of tauopathies. Interestingly, tau hyperphosphorylation begins in different regions of the brain in each tauopathy. In some regions, both neurons and glial cells develop tau hyperphosphorylation. Tau hyperphosphorylation is also observed in physiological conditions such as hibernation and brain development. In the first section of present article, we will review the spatiotemporal and cellular distribution of hyperphosphorylated tau in the most frequent tauopathies. In the second section, we will compare the pattern of tau hyperphosphorylation in physiological and pathological conditions and discuss the sites that could play a pivotal role in the conversion of non-toxic to toxic forms of hyperphosphorylated tau. Furthermore, we will discuss the role of hyperphosphorylated tau in physiological and pathological conditions and the fact that tau hyperphosphorylation is reversible in physiological conditions but not in a pathological ones. In the third section, we will speculate how the differences and similarities between hyperphosphorylated tau in physiological and pathological conditions could impact the elaboration of therapies to prevent tau pathology. In the fourth section, the different therapeutic approaches using tau as a direct or indirect therapeutic target will be presented.

Recent Advances in Molecular Hydrogen Research Reducing Exercise-Induced Oxidative Stress and Inflammation

2020 ◽  
Vol 26 ◽  
Author(s):  
Jonatas E. Nogueira ◽  
Luiz G. S. Branco
Keyword(s):  
Oxidative Stress ◽  
Physical Exercise ◽  
Molecular Hydrogen ◽  
Current Knowledge ◽  
Human Studies ◽  
Physiological Conditions ◽  
Pathological Conditions ◽  
Inflammatory Molecule ◽  
Exercise Induced ◽  
Reporting Data

: Physical exercise-induced oxidative stress and inflammation may be beneficial when exercise is a regular activity, but it is rather harmful when exercise is exhaustive and performed by unaccustomed organisms. Molecular hydrogen (H2 ) has recently appeared as a potent antioxidant and anti-inflammatory molecule in numerous pathological conditions. However, its role is relatively unknown under physiological conditions such as physical exercise. Therefore, this review summarizes the current knowledge of the H2 reducing oxidative stress and inflammation in physical exercise, reporting data from both animal and human studies.

scholarly journals Glutathione in multiple sclerosis: More than just an antioxidant?

2014 ◽  
Vol 20 (11) ◽  
pp. 1425-1431 ◽  
Author(s):  
Andreia N Carvalho ◽  
Jamie L Lim ◽  
Philip G Nijland ◽  
Maarten E Witte ◽  
Jack Van Horssen
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Therapeutic Potential ◽  
Comprehensive Overview ◽  
Non Invasive ◽  
Gsh Metabolism ◽  
Reactive Oxidants ◽  
Antioxidant Mechanisms ◽  
The Brain

Oxidative stress has been strongly implicated in both the inflammatory and neurodegenerative pathological mechanisms in multiple sclerosis (MS). In response to oxidative stress, cells increase and activate their cellular antioxidant mechanisms. Glutathione (GSH) is the major antioxidant in the brain, and as such plays a pivotal role in the detoxification of reactive oxidants. Previous research has shown that GSH homeostasis is altered in MS. In this review, we provide a comprehensive overview on GSH metabolism in brain cells, with a focus on its involvement in MS. The potential of GSH as an in vivo biomarker in MS is discussed, along with a short overview of improvements in imaging methods that allow non-invasive quantification of GSH in the brain. These methods might be instrumental in providing real-time measures of GSH, allowing the assessment of the oxidative state in MS patients and the monitoring of disease progression. Finally, the therapeutic potential of GSH in MS is discussed.

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