scholarly journals Non-Coding RNAs as Sensors of Oxidative Stress in Neurodegenerative Diseases

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1095
Author(s):  
Ana Gámez-Valero ◽  
Anna Guisado-Corcoll ◽  
Marina Herrero-Lorenzo ◽  
Maria Solaguren-Beascoa ◽  
Eulàlia Martí
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nervous System ◽  
Neurodegenerative Diseases ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Normal Function ◽  
Brain Cell ◽  
Oxygen Species ◽  
Age Related

Oxidative stress (OS) results from an imbalance between the production of reactive oxygen species and the cellular antioxidant capacity. OS plays a central role in neurodegenerative diseases, where the progressive accumulation of reactive oxygen species induces mitochondrial dysfunction, protein aggregation and inflammation. Regulatory non-protein-coding RNAs (ncRNAs) are essential transcriptional and post-transcriptional gene expression controllers, showing a highly regulated expression in space (cell types), time (developmental and ageing processes) and response to specific stimuli. These dynamic changes shape signaling pathways that are critical for the developmental processes of the nervous system and brain cell homeostasis. Diverse classes of ncRNAs have been involved in the cell response to OS and have been targeted in therapeutic designs. The perturbed expression of ncRNAs has been shown in human neurodegenerative diseases, with these changes contributing to pathogenic mechanisms, including OS and associated toxicity. In the present review, we summarize existing literature linking OS, neurodegeneration and ncRNA function. We provide evidences for the central role of OS in age-related neurodegenerative conditions, recapitulating the main types of regulatory ncRNAs with roles in the normal function of the nervous system and summarizing up-to-date information on ncRNA deregulation with a direct impact on OS associated with major neurodegenerative conditions.

scholarly journals Resistance of nerve cells to oxidative injury

2011 ◽  
Vol 64 (7-8) ◽  
pp. 386-391 ◽  
Author(s):  
Zorica Jovanovic ◽  
Svetlana Jovanovic
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Neuronal Damage ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Brain Cell ◽  
Nerve Cells ◽  
Oxygen Species ◽  
The Brain

Introduction. Reactive oxygen species are particularly active in the brain and neuronal tissue, and they are involved in numerous cellular functions, including cell death and survival. Brain and oxidative stress. A high metabolic rate and an abundant supply of the transition metals make the brain an ideal target for a free radical attack. In addition, the brain has a high susceptibility to oxidative stress due to the high lipid content and relatively lower regenerative capacity in comparison with other tissues. Vulnerability of nerve cells to oxidative stress. The neurons are more vulnerable to oxidative stress than other brain cell types. In addition to the two conventional enzymes, catalase and glutathione peroxidase, peroxiredoxins remove intracellular hydrogen peroxide by reducing it to water. The recent work increasingly supports the hypothesis that peroxiredoxins are not only antioxidant proteins, but they also play a role in cell signaling by controlling hydrogen peroxide and alkyl hydroperoxide levels. The accumulating evidence demonstrates that microglia can become deleterious and damage neurons. The overactivated microglia release reactive oxygen species that cause neuronal damage in neurodegenerative diseases. Conclusion. The defense of nerve cells against reactive oxygen species - mediated oxidative damage is essential for maintaining the functionality of nerve cells. The ongoing studies show that neuron-glial compartmentalization of antioxidants is critical for the neuronal signaling by hydrogen peroxide as well as the neuronal protection.

scholarly journals Effects of Aging on Cardiac Oxidative Stress and Transcriptional Changes in Pathways of Reactive Oxygen Species Generation and Clearance

2021 ◽  
Author(s):  
Farhan Rizvi ◽  
Claudia C. Preston ◽  
Larisa Emelyanova ◽  
Mohammed Yousufuddin ◽  
Maria Viqar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Complex I ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Functional Enrichment ◽  
Pathway Enrichment Analysis ◽  
Oxygen Species ◽  
Age Related ◽  
Ros Homeostasis

Background Age‐related heart diseases are significant contributors to increased morbidity and mortality. Emerging evidence indicates that mitochondria within cardiomyocytes contribute to age‐related increased reactive oxygen species (ROS) generation that plays an essential role in aging‐associated cardiac diseases. Methods and Results The present study investigated differences between ROS production in cardiomyocytes isolated from adult (6 months) and aged (24 months) Fischer 344 rats, and in cardiac tissue of adult (18–65 years) and elderly (>65 years) patients with preserved cardiac function. Superoxide dismutase inhibitable ferricytochrome c reduction assay (1.32±0.63 versus 0.76±0.31 nMol/mg per minute; P =0.001) superoxide and H 2 O 2 production, measured as dichlorofluorescein diacetate fluorescence (1646±428 versus 699±329, P =0.04), were significantly higher in the aged versus adult cardiomyocytes. Similarity in age‐related alteration between rats and humans was identified in mitochondrial‐electron transport chain‐complex‐I‐associated increased oxidative‐stress by MitoSOX fluorescence (53.66±18.58 versus 22.81±12.60; P =0.03) and in 4‐HNE adduct levels (187.54±54.8 versus 47.83±16.7 ng/mg protein, P =0.0063), indicative of increased peroxidation in the elderly. These differences correlated with changes in functional enrichment of genes regulating ROS homeostasis pathways in aged human and rat hearts. Functional merged collective network and pathway enrichment analysis revealed common genes prioritized in human and rat aging‐associated networks that underlay enriched functional terms of mitochondrial complex I and common pathways in the aging human and rat heart. Conclusions Aging sensitizes mitochondrial and extramitochondrial mechanisms of ROS buildup within the heart. Network analysis of the transcriptome highlights the critical elements involved with aging‐related ROS homeostasis pathways common in rat and human hearts as targets.

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.

Oxidation of Potassium Channels in Neurodegenerative Diseases: A Mini- Review

2018 ◽  
Vol 17 (4) ◽  
pp. 267-271 ◽  
Author(s):  
Junsheng Yang ◽  
Xueni Yan
Keyword(s):  
Reactive Oxygen Species ◽  
Central Nervous System ◽  
Nervous System ◽  
Potassium Channels ◽  
Oxidative Damage ◽  
Neurodegenerative Diseases ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cell Functions ◽  
The Central Nervous System

Background & Objective: Increased level of reactive oxygen species is a hallmark of common neurodegenerative diseases such as Alzheimer’s Disease and Parkinson’s Disease. ROS can oxidize macromolecules including DNA, lipids and proteins and cause oxidative damage to the cell. Emerging evidence indicate that potassium channels in the central nervous system are no exceptions to these oxidative modifications. Conclusion: In this mini-review, we summarized recent reports on the oxidation of potassium channels in the CNS and the consequently resulted changes in cell functions and viability, with focus on its implications in neurodegenerative diseases.

scholarly journals Transducing oxidative stress to death signals in neurons

2015 ◽  
Vol 211 (4) ◽  
pp. 741-743 ◽  
Author(s):  
Xu Cao ◽  
Yanshan Fang
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Neurodegenerative Diseases ◽  
Neuronal Apoptosis ◽  
Axonal Degeneration ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cell Biol ◽  
Death Signals

Accumulation of reactive oxygen species (ROS) has been associated with aging and neurodegenerative diseases. Nevertheless, how elevated ROS levels cause neurodegeneration is unclear. In this issue, Wakatsuki et al. (2015. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201506102) delineate how oxidative stress is transduced into death signals, leading to neuronal apoptosis and axonal degeneration.

Oxidative stress and reactive oxygen species: a review of their role in ocular disease

2017 ◽  
Vol 131 (24) ◽  
pp. 2865-2883 ◽  
Author(s):  
Lawson Ung ◽  
Ushasree Pattamatta ◽  
Nicole Carnt ◽  
Jennifer L. Wilkinson-Berka ◽  
Gerald Liew ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Function ◽  
Physiological Role ◽  
Reactive Oxygen ◽  
Age Related Macular Degeneration ◽  
Current Evidence ◽  
Oxygen Species ◽  
Age Related

For many years, oxidative stress arising from the ubiquitous production of reactive oxygen species (ROS) has been implicated in the pathogenesis of various eye diseases. While emerging research has provided some evidence of the important physiological role of ROS in normal cell function, disease may arise where the concentration of ROS exceeds and overwhelms the body’s natural defence against them. Additionally, ROS may induce genomic aberrations which affect cellular homoeostasis and may result in disease. This literature review examines the current evidence for the role of oxidative stress in important ocular diseases with a view to identifying potential therapeutic targets for future study. The need is particularly pressing in developing treatments for conditions which remain notoriously difficult to treat, including glaucoma, diabetic retinopathy and age-related macular degeneration.

scholarly journals Role of Melanin in Melanocyte Dysregulation of Reactive Oxygen Species

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Noah C. Jenkins ◽  
Douglas Grossman
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Oxygen Species ◽  
Intracellular Ros ◽  
Potential Alternative ◽  
Oxidative Insult ◽  
Increased Susceptibility

We have recently reported a potential alternative tumor suppressor function for p16 relating to its capacity to regulate oxidative stress and observed that oxidative dysregulation in p16-depleted cells was most profound in melanocytes, compared to keratinocytes or fibroblasts. Moreover, in the absence of p16 depletion or exogenous oxidative insult, melanocytes exhibited significantly higher basal levels of reactive oxygen species (ROS) than these other epidermal cell types. Given the role of oxidative stress in melanoma development, we speculated that this increased susceptibility of melanocytes to oxidative stress (and greater reliance on p16 for suppression of ROS) may explain why genetic compromise of p16 is more commonly associated with predisposition to melanoma rather than other cancers. Here we show that the presence of melanin accounts for this differential oxidative stress in normal and p16-depleted melanocytes. Thus the presence of melanin in the skin appears to be a double-edged sword: it protects melanocytes as well as neighboring keratinocytes in the skin through its capacity to absorb UV radiation, but its synthesis in melanocytes results in higher levels of intracellular ROS that may increase melanoma susceptibility.

scholarly journals Reactive Oxygen Species-Mediated Damage of Retinal Neurons: Drug Development Targets for Therapies of Chronic Neurodegeneration of the Retina

2018 ◽  
Vol 19 (11) ◽  
pp. 3362 ◽  
Author(s):  
Landon Rohowetz ◽  
Jacob Kraus ◽  
Peter Koulen
Keyword(s):  
Reactive Oxygen Species ◽  
Neurodegenerative Diseases ◽  
Reactive Oxygen ◽  
Age Related Macular Degeneration ◽  
Oxygen Species ◽  
Treatment And Prevention ◽  
Age Related ◽  
Recent Developments ◽  
Low Levels

The significance of oxidative stress in the development of chronic neurodegenerative diseases of the retina has become increasingly apparent in recent years. Reactive oxygen species (ROS) are free radicals produced at low levels as a result of normal cellular metabolism that are ultimately metabolized and detoxified by endogenous and exogenous mechanisms. In the presence of oxidative cellular stress, ROS are produced in excess, resulting in cellular injury and death and ultimately leading to tissue and organ dysfunction. Recent studies have investigated the role of excess ROS in the pathogenesis and development of chronic neurodegenerative diseases of the retina including glaucoma, diabetic retinopathy, and age-related macular degeneration. Findings from these studies are promising insofar as they provide clear rationales for innovative treatment and prevention strategies of these prevalent and disabling diseases where currently therapeutic options are limited. Here, we briefly outline recent developments that have contributed to our understanding of the role of ROS in the pathogenesis of chronic neurodegenerative diseases of the retina. We then examine and analyze the peer-reviewed evidence in support of ROS as targets for therapy development in the area of chronic neurodegeneration of the retina.

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