scholarly journals Interaction of Oxidative Stress and Misfolded Proteins in the Mechanism of Neurodegeneration

Life ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 101 ◽  
Author(s):  
Andrey Y. Abramov ◽  
Elena V. Potapova ◽  
Viktor V. Dremin ◽  
Andrey V. Dunaev
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Neurodegenerative Disorders ◽  
Structural Changes ◽  
Wide Spectrum ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Misfolded Proteins ◽  
Oxygen Species

Aggregation of the misfolded proteins β-amyloid, tau, huntingtin, and α-synuclein is one of the most important steps in the pathology underlying a wide spectrum of neurodegenerative disorders, including the two most common ones—Alzheimer’s and Parkinson’s disease. Activity and toxicity of these proteins depends on the stage and form of aggregates. Excessive production of free radicals, including reactive oxygen species which lead to oxidative stress, is proven to be involved in the mechanism of pathology in most of neurodegenerative disorders. Both reactive oxygen species and misfolded proteins play a physiological role in the brain, and only deregulation in redox state and aggregation of the proteins leads to pathology. Here, we review the role of misfolded proteins in the activation of ROS production from various sources in neurons and glia. We discuss if free radicals can influence structural changes of the key toxic intermediates and describe the putative mechanisms by which oxidative stress and oligomers may cause neuronal death.

scholarly journals Reactive Oxygen Species Regulate Activity-Dependent Neuronal Structural Plasticity in Drosophila

2016 ◽  
Author(s):  
Matthew C. W. Oswald ◽  
Paul S. Brooks ◽  
Maarten F. Zwart ◽  
Amrita Mukherjee ◽  
Ryan J. H. West ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Structural Changes ◽  
Second Messengers ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Structural Plasticity ◽  
Activity Level ◽  
Oxygen Species ◽  
Network Output ◽  
Activity Dependent

AbstractNeurons are inherently plastic, adjusting their structure, connectivity and excitability in response to changes in activity. How neurons sense changes in their activity level and then transduce these to structural changes remains to be fully elucidated. Working with the Drosophila larval locomotor network, we show that neurons use reactive oxygen species (ROS), metabolic byproducts, to monitor their activity. ROS signals are both necessary and sufficient for activity-dependent structural adjustments of both pre- and postsynaptic terminals and for network output, as measured by larval crawling behavior. We find the highly conserved Parkinson’s disease-linked protein DJ-1ß acts as a redox sensor in neurons where it regulates pre- and postsynaptic structural plasticity, in part via modulation of the PTEN-PI3Kinase pathway. Neuronal ROS thus play an important physiological role as second messengers required for neuronal and network tuning, whose dysregulation in the ageing brain and under neurodegenerative conditions may contribute to synaptic dysfunction.

The effect of ethanol on the development of oxidative stress and endothelial dysfunction

2020 ◽  
Vol 21 (3) ◽  
pp. 143-149
Author(s):  
I. A. Chernov ◽  
◽  
Yu. A. Kirillov ◽  
D. A. Areshidze ◽  
M. A. Kozlova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Structural Changes ◽  
Alcohol Intoxication ◽  
Reactive Oxygen ◽  
The Body ◽  
Oxygen Species ◽  
Electron Microscopic ◽  
Small Doses

The review focuses on the pathogenetic mechanisms of ethanol influence on the development of oxidative stress (OS) and endothelial dysfunction (ED). It is shown that both in acute and chronic alcohol intoxication, the intake of ethanol in the body initiates the development of OS, the formation of reactive oxygen species, causes a decrease in the content of endothelium-derived relaxing factors (nitric oxide (NO), prostacyclin, endothelium-derived hyperpolarization factor (EDHF)), an increase in the concentration of endothelium-derived constricting factors (endothelin, angiotensin-II), thereby causing the development of ED. When alcohol is consumed in small doses by healthy non-drinkers, ethanol can act as an antioxidant, cause the neutralization of reactive oxygen species, promote the formation of NO, and prevent the formation of ED. Currently used methods for evaluating ED allow us to characterize the functional state of the endothelium. Structural changes in the blood vessel wall as a manifestation of ED in alcoholic disease are not sufficiently described, which indicates the need to study them using modern histological, histochemical, immunohistochemical and electron microscopic methods.

scholarly journals Mechanism of Oxidative Stress in Neurodegeneration

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Sonia Gandhi ◽  
Andrey Y. Abramov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Neurodegenerative Disease ◽  
Reactive Oxygen ◽  
Biological Tissues ◽  
Antioxidant Systems ◽  
Oxygen Species

Biological tissues require oxygen to meet their energetic demands. However, the consumption of oxygen also results in the generation of free radicals that may have damaging effects on cells. The brain is particularly vulnerable to the effects of reactive oxygen species due to its high demand for oxygen, and its abundance of highly peroxidisable substrates. Oxidative stress is caused by an imbalance in the redox state of the cell, either by overproduction of reactive oxygen species, or by dysfunction of the antioxidant systems. Oxidative stress has been detected in a range of neurodegenerative disease, and emerging evidence from in vitro and in vivo disease models suggests that oxidative stress may play a role in disease pathogenesis. However, the promise of antioxidants as novel therapies for neurodegenerative diseases has not been borne out in clinical studies. In this review, we critically assess the hypothesis that oxidative stress is a crucial player in common neurodegenerative disease and discuss the source of free radicals in such diseases. Furthermore, we examine the issues surrounding the failure to translate this hypothesis into an effective clinical treatment.

scholarly journals The Free Radical Theory of Aging and Antioxidant Supplements

2012 ◽  
Vol 17 (3) ◽  
pp. 218-220
Author(s):  
Bruce A. Buehler
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Free Radical ◽  
Life Span ◽  
Reactive Oxygen ◽  
Cell Aging ◽  
Oxygen Species ◽  
Radical Theory ◽  
Antioxidant Supplements

Free radical excess occurs when cells are exposed to reactive oxygen species greater than the amount that can be neutralized by cellular produced antioxidants such as superoxide dismutase. This is termed oxidative stress, which can be caused by excessive energy intake or external pollutants. Excess free radicals are proposed to increase the rate of cell aging, injury, and mutations leading to a shortened cell life span. Vitamins A, C, and E and flavoproteins are supplements that function as free radical scavengers. Antioxidants are present in natural foods but added amounts beyond the diet may detoxify excess free radicals during “oxidative stress.” Antioxidant supplements decrease cellular damage from excess reactive oxygen species but they have not been proven to prolong life span.

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 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.

Association of Oxidative Stress with Neurological Disorders

2021 ◽  
Vol 19 ◽  
Author(s):  
Waseem Hassan ◽  
Hamsa Noreen ◽  
Shakila Rehman ◽  
Mohammad Amjad Kamal ◽  
Joao Batista Teixeira da Rocha
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Neurodegenerative Diseases ◽  
Neurological Disorders ◽  
Biological Effects ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Neuronal Membranes

Background: Oxidative stress is one of the main contributing factors involved in cerebral biochemical impairment. The higher susceptibility of the central nervous system to reactive oxygen species mediated damage could be attributed to several factors. For example, neurons use a greater quantity of oxygen, many parts of the brain have higher concentraton of iron, and neuronal mitochondria produce huge content of hydrogen peroxide. In addition, neuronal membranes have polyunsaturated fatty acids, which are predominantly vulnerable to oxidative stress (OS). OS is the imbalance between reactive oxygen species generation and cellular antioxidant potential. This may lead to various pathological conditions and diseases, especially neurodegenerative diseases such as, Parkinson’s, Alzheimer’s, and Huntington’s diseases. Objectives: In this study, we explored the involvement of OS in neurodegenerative diseases. Methods: We used different search terms like “oxidative stress and neurological disorders” “free radicals and neurodegenerative disorders” “oxidative stress, free radicals, and neurological disorders” and “association of oxidative stress with the name of disorders taken from the list of neurological disorders. We tried to summarize the source, biological effects, and physiologic functions of ROS. Results: Finally, it was noted that more than 190 neurological disorders are associated with oxidative stress.

Ovariectomy and its Antioxidative Effect on Bone

2010 ◽  
Author(s):  
Durg V. Rai ◽  
Harcharan Singh Ranu
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Bone Loss ◽  
Wistar Rats ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Female Wistar Rats ◽  
The Impact

Ovarian hormone deficiency increases the generation of reactive oxygen species. Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. There is increasing evidence of the role of free radicals in bone resorption and bone loss. Ovariectomised female wistar rats had been used as the animal model for the study of osteoporosis. Even though, there are studies portraying the role of free radicals in bone loss, the defense mechanism adapted by bone in ovariectomised animals remains obscure. So, the impact of ovariectomy on the bone antioxidant system in rats was investigated. Twenty female wistar rats were taken and divided into two groups: ovariectomised and control. It had been found that a significant (p<0.001) decrease in the activity of various enzymes like CAT (catalase), SOD (superoxide dismutase) (p<0.001), GST (glutathione-s-transferase). However, an increase in the malondialdehyde levels was found to be 30% in the ovariectomised rats as compared to the controls. Thus the study elucidates the oxidative stress in bone under ovariectomy.

Oxidative Stress, Antioxidant Status, and the Contracting Diaphragm

1998 ◽  
Vol 23 (1) ◽  
pp. 23-55 ◽  
Author(s):  
John M. Lawler ◽  
Scott K. Powers
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Membrane Lipids ◽  
Reactive Oxygen ◽  
Respiratory Muscles ◽  
Strenuous Exercise ◽  
Antioxidant Enzyme Activities ◽  
Key Words Aging ◽  
Oxygen Species

Reactive oxygen species, including free radicals, are produced through a number of biochemical reactions, often as a consequence of aerobic metabolism. A system of antioxidant enzymes and scavenger substrates provides protection of membrane lipids, proteins, and DNA. An imbalance between production of reactive oxygen species and antioxidant protection results in "oxidative stress." Oxidative stress is believed to contribute to numerous pathological conditions including atherosclerosis, obstructive lung disease, aging, and fatigue of skeletal muscles including the diaphragm. Strenuous exercise, inflammation, infection, obstructive lung diseases, etc. increase exposure of the diaphragm to reactive oxygen species. Emerging data indicate that reactive oxygen species alter diaphragm contractions primarily in response to low-frequency stimulation. The response of the diaphragm is profoundly influenced by the degree of oxidative stress, fatigue state, glutathione status, and age. Exercise training results in an upregulation of antioxidant enzyme activities in the diaphragm and thus could provide additional protection against oxidative stress. Key words: aging, excitation-contraction coupling, exercise, fatigue, free radicals, glutathione peroxidase, oxidation/reduction, reactive oxygen species, respiratory muscles, skeletal muscle, superoxide dismutase

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