scholarly journals Oxidative Stress and Neuroinflammation Potentiate Each Other to Promote Progression of Dopamine Neurodegeneration

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Jingyi He ◽  
Guofu Zhu ◽  
Guoqing Wang ◽  
Feng Zhang
Keyword(s):  
Oxidative Stress ◽  
Complex Disease ◽  
Lewy Bodies ◽  
Oxygen Species ◽  
Independent Factor ◽  
Internal Environment ◽  
Progressive Loss ◽  
Entry Points ◽  
Toxic Environment ◽  
The Central Nervous System

Parkinson’s disease (PD) is a chronic and complex disease of the central nervous system (CNS). Progressive loss of dopamine (DA) neurons in midbrain substantia nigra is considered to be the main cause of PD. The hallmark of PD pathology is the formation of Lewy bodies and the deposition of α-synuclein (α-syn). The mechanisms responsible for the progressive feature of DA neurodegeneration are not fully illustrated. Recently, oxidative stress and neuroinflammation have received extensive attention as two important entry points in the pathogenesis of PD. The occurrence of oxidative stress and neuroinflammation is usually derived from external influences or changes in internal environment, such as the accumulation of reactive oxygen species, exposure to a toxic environment, and the transformation of systemic inflammation. However, PD never results from a single independent factor and the simultaneous participation of oxidative stress and neuroinflammation contributed to PD development. Oxidative stress and neuroinflammation could potentiate each other to promote progression of PD. In this review, we briefly summarized the conditions of oxidative stress and neuroinflammation and the crosstalk between oxidative stress and neuroinflammation on the development of PD.

scholarly journals Mini-Review on Lipofuscin and Aging: Focusing on The Molecular Interface, The Biological Recycling Mechanism, Oxidative Stress, and The Gut-Brain Axis Functionality

Medicina ◽  
2020 ◽  
Vol 56 (11) ◽  
pp. 626
Author(s):  
Ovidiu-Dumitru Ilie ◽  
Alin Ciobica ◽  
Sorin Riga ◽  
Nitasha Dhunna ◽  
Jack McKenna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Internal Environment ◽  
Antagonistic Effects ◽  
Lysosomal Accumulation ◽  
The Central Nervous System ◽  
Biological Recycling

Intra-lysosomal accumulation of the autofluorescent “residue” known as lipofuscin, which is found within postmitotic cells, remains controversial. Although it was considered a harmless hallmark of aging, its presence is detrimental as it continually accumulates. The latest evidence highlighted that lipofuscin strongly correlates with the excessive production of reactive oxygen species; however, despite this, lipofuscin cannot be removed by the biological recycling mechanisms. The antagonistic effects exerted at the DNA level culminate in a dysregulation of the cell cycle, by inducing a loss of the entire internal environment and abnormal gene(s) expression. Additionally, it appears that a crucial role in the production of reactive oxygen species can be attributed to gut microbiota, due to their ability to shape our behavior and neurodevelopment through their maintenance of the central nervous system.

scholarly journals Oxidative Stress Inside the Pathogenesis of Ascending Aorta Aneurysms: A Clearer Vision for Identifying Promising Biomarkers and Therapeutic Targets

2021 ◽  
Author(s):  
Carmela Balistreri ◽  
Calogera Pisano ◽  
Giovanni Ruvolo
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Genetic Variants ◽  
Complex Disease ◽  
Ascending Aorta ◽  
Oxygen Species ◽  
Aorta Aneurysm ◽  
Independent Risk Factors ◽  
The Impact ◽  
And Oxidative Stress

Ascending aorta aneurysm (AsAA) is a complex disease, currently defined an inflammatory disease. In the sporadic form, AsAA has, indeed, a complex physiopathology with a strong inflammatory basis, significantly modulated by genetic variants in innate/inflammatory genes, acting as independent risk factors and as largely evidenced in our recent studies performed during the last 10 years. Based on these premises, here, we want to revise the impact of reactive oxygen species (ROS) and oxidative stress on AsAA pathophysiology and consequently on the onset and progression of sporadic AsAA. This might consent to add other important pieces in the intricate puzzle of the pathophysiology of this disease with the translational aim to identify biomarkers and targets to apply in the complex management of AsAA, by facilitating the AsAA diagnosis currently based only on imaging evaluations, and the treatment exclusively founded on surgery approaches.

scholarly journals A Review of Various Antioxidant Compounds and their Potential Utility as Complementary Therapy in Multiple Sclerosis

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1528 ◽  
Author(s):  
Elzbieta Dorota Miller ◽  
Angela Dziedzic ◽  
Joanna Saluk-Bijak ◽  
Michal Bijak
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Complex Disease ◽  
Early Stage ◽  
Symptomatic Treatment ◽  
Complementary Therapy ◽  
Antioxidant Compounds ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
Stress Mediators

Multiple sclerosis (MS) is a complex disease of the central nervous system (CNS). The etiology of this multifactorial disease has not been clearly defined. Conventional medical treatment of MS has progressed, but is still based on symptomatic treatment. One of the key factors in the pathogenesis of MS is oxidative stress, enhancing inflammation and neurodegeneration. In MS, both reactive oxygen and nitrogen species are formed in the CNS mainly by activated macrophages and microglia structures, which can lead to demyelination and axon disruption. The course of MS is associated with the secretion of many inflammatory and oxidative stress mediators, including cytokines (IL-1b, IL-6, IL-17, TNF-α, INF-γ) and chemokines (MIP-1a, MCP-1, IP10). The early stage of MS (RRMS) lasts about 10 years, and is dominated by inflammatory processes, whereas the chronic stage is associated with neurodegenerative axon and neuron loss. Since oxidative damage has been known to be involved in inflammatory and autoimmune-mediated processes, antioxidant therapy could contribute to the reduction or even prevention of the progression of MS. Further research is needed in order to establish new aims for novel treatment and provide possible benefits to MS patients. The present review examines the roles of oxidative stress and non-pharmacological anti-oxidative therapies in MS.

scholarly journals Lipid-Mediated Oxidative Stress and Inflammation in the Pathogenesis of Parkinson's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Tahira Farooqui ◽  
Akhlaq A. Farooqui
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Platelet Activating Factor ◽  
Lipid Mediators ◽  
Unknown Etiology ◽  
Oxygen Species ◽  
Progressive Loss ◽  
Progressive Neurodegeneration

Parkinson's disease (PD) is a neurodegenerative movement disorder of unknown etiology. PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, depletion of dopamine in the striatum, abnormal mitochondrial and proteasomal functions, and accumulation ofα-synuclein that may be closely associated with pathological and clinical abnormalities. Increasing evidence indicates that both oxidative stress and inflammation may play a fundamental role in the pathogenesis of PD. Oxidative stress is characterized by increase in reactive oxygen species (ROS) and depletion of glutathione. Lipid mediators for oxidative stress include 4-hydroxynonenal, isoprostanes, isofurans, isoketals, neuroprostanes, and neurofurans. Neuroinflammation is characterized by activated microglial cells that generate proinflammatory cytokines, such as TNF-αand IL-1β. Proinflammatory lipid mediators include prostaglandins and platelet activating factor, together with cytokines may play a prominent role in mediating the progressive neurodegeneration in PD.

scholarly journals Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

2020 ◽  
Vol 10 (10) ◽  
pp. 742
Author(s):  
Samskruthi Madireddy ◽  
Sahithi Madireddy
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Defense Mechanism ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Progressive Development ◽  
The Central Nervous System ◽  
Cognitive Therapies ◽  
Nutritional Strategies

The biochemical integrity of the brain is paramount to the function of the central nervous system, and oxidative stress is a key contributor to cerebral biochemical impairment. Oxidative stress, which occurs when an imbalance arises between the production of reactive oxygen species (ROS) and the efficacy of the antioxidant defense mechanism, is believed to play a role in the pathophysiology of various brain disorders. One such disorder, schizophrenia, not only causes lifelong disability but also induces severe emotional distress; however, because of its onset in early adolescence or adulthood and its progressive development, consuming natural antioxidant products may help regulate the pathogenesis of schizophrenia. Therefore, elucidating the functions of ROS and dietary antioxidants in the pathogenesis of schizophrenia could help formulate improved therapeutic strategies for its prevention and treatment. This review focuses specifically on the roles of ROS and oxidative damage in the pathophysiology of schizophrenia, as well as the effects of nutrition, antipsychotic use, cognitive therapies, and quality of life on patients with schizophrenia. By improving our understanding of the effects of various nutrients on schizophrenia, it may become possible to develop nutritional strategies and supplements to treat the disorder, alleviate its symptoms, and facilitate long-term recovery.

scholarly journals Rationale for Antioxidant Supplementation in Sarcopenia

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Francesco Cerullo ◽  
Giovanni Gambassi ◽  
Matteo Cesari
Keyword(s):  
Oxidative Stress ◽  
Muscle Function ◽  
Molecular Mechanisms ◽  
Motor Units ◽  
Oxygen Species ◽  
Antioxidant Supplementation ◽  
Present Evidence ◽  
Progressive Loss ◽  
Age Related ◽  
Prevention And Treatment

Sarcopenia is an age-related clinical condition characterized by the progressive loss of motor units and wasting of muscle fibers resulting in decreased muscle function. The molecular mechanisms leading to sarcopenia are not completely identified, but the increased oxidative damage occurring in muscle cells during the course of aging represents one of the most accepted underlying pathways. In fact, skeletal muscle is a highly oxygenated tissue and the generation of reactive oxygen species is particularly enhanced in both contracting and at rest conditions. It has been suggested that oral antioxidant supplementation may contribute at reducing indices of oxidative stress both in animal and human models by reinforcing the natural endogenous defenses. Aim of the present paper is to discuss present evidence related to possible benefits of oral antioxidants in the prevention and treatment of sarcopenia.

scholarly journals Relevance of the Glutathione System in Temporal Lobe Epilepsy: Evidence in Human and Experimental Models

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Noemí Cárdenas-Rodríguez ◽  
Elvia Coballase-Urrutia ◽  
Claudia Pérez-Cruz ◽  
Hortencia Montesinos-Correa ◽  
Liliana Rivera-Espinosa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Experimental Models ◽  
Oxygen Species ◽  
Glutathione System ◽  
Biochemical Status ◽  
The Central Nervous System ◽  
Biochemical State

Oxidative stress, which is a state of imbalance in the production of reactive oxygen species and nitrogen, is induced by a wide variety of factors. This biochemical state is associated with diseases that are systemic as well as diseases that affect the central nervous system. Epilepsy is a chronic neurological disorder, and temporal lobe epilepsy represents an estimated 40% of all epilepsy cases. Currently, evidence from human and experimental models supports the involvement of oxidative stress during seizures and in the epileptogenesis process. Hence, the aim of this review was to provide information that facilitates the processing of this evidence and investigate the therapeutic impact of the biochemical status for this specific pathology.

scholarly journals Oxidative Stress in Multiple Sclerosis Disease (Review Article)

2021 ◽  
Vol 21 (2) ◽  
pp. 33-40
Author(s):  
Sura Mohammed Kadhim ◽  
◽  
Sura Mohsin Abbood ◽  
Yasser Mohammed Taay ◽  
Mustafa Taha Mohammed
Keyword(s):  
Oxidative Stress ◽  
Multiple Sclerosis ◽  
Living System ◽  
Review Article ◽  
Oxygen Species ◽  
Myelin Sheaths ◽  
Multiple Sclerosis Disease ◽  
The Central Nervous System ◽  
Keywords Oxidative Stress ◽  
And Oxidative Stress

Background: Multiple sclerosis (MS) is an inflammatory disease of the central nervous system, in which the myelin sheaths got injured. The prevalence of MS is on grow, as well as, it affects the young ages. Females are most common to have MS compared to males. Oxidative stress is the situation of imbalance between oxidants (free radicals and reactive oxygen species (ROS)) and antioxidants in a living system, in which either the oxidants are elevated or antioxidants are reduced, or sometimes both. ROS and oxidative stress have been implicated in the progression of many degenerative diseases, which is important in cracking the unrevealed mysteries of MS. In this review article, some of the proposed mechanisms that link oxidative stress with MS disease would be described. Keywords: Oxidative stress, ROS, multiple sclerosis, antioxidants

scholarly journals NADPH Oxidase: A Potential Target for Treatment of Stroke

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Li Zhang ◽  
Jie Wu ◽  
Xiaochun Duan ◽  
Xiaodi Tian ◽  
Haitao Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Physiological Function ◽  
Neuroprotective Effect ◽  
Experimental Stroke ◽  
Oxygen Species ◽  
Industrialized Nations ◽  
Nox Inhibitors ◽  
Stroke Models ◽  
The Central Nervous System

Stroke is the third leading cause of death in industrialized nations. Oxidative stress is involved in the pathogenesis of stroke, and excessive generation of reactive oxygen species (ROS) by mitochondria is thought to be the main cause of oxidative stress. NADPH oxidase (NOX) enzymes have recently been identified and studied as important producers of ROS in brain tissues after stroke. Several reports have shown that knockout or deletion of NOX exerts a neuroprotective effect in three major experimental stroke models. Recent studies also confirmed that NOX inhibitors ameliorate brain injury and improve neurological outcome after stroke. However, the physiological and pathophysiological roles of NOX enzymes in the central nervous system (CNS) are not known well. In this review, we provide a comprehensive summary of our current understanding about expression and physiological function of NOX enzymes in the CNS and its pathophysiological roles in the three major types of stroke: ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage.

scholarly journals Nose-to-Brain Delivery of Antioxidants as a Potential Tool for the Therapy of Neurological Diseases

Pharmaceutics ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 1246
Author(s):  
Maria Cristina Bonferoni ◽  
Giovanna Rassu ◽  
Elisabetta Gavini ◽  
Milena Sorrenti ◽  
Laura Catenacci ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Diseases ◽  
Olfactory Nerve ◽  
Brain Targeting ◽  
Brain Delivery ◽  
Oxygen Species ◽  
Neuroprotective Effects ◽  
The Central Nervous System ◽  
The Brain ◽  
Potential Tool

Oxidative stress has a key role in the pathogenesis of neurodegenerative disorders such as Alzheimer’s, Parkinson’s, and Huntington’s diseases and can be an important cause of the damages in cerebral ischemia. Oxidative stress arises from high levels of reactive oxygen species (ROS). Consequently, on this rational base, antioxidants (many of natural origin) are proposed as potential drugs to prevent ROS noxious actions because they can protect the target tissues from the oxidative stress. However, the potential of antioxidants is limited, owing to the presence of the blood–brain barrier (BBB), which is difficult to cross with a consequent low bioavailability of the drug into the brain after systemic (intravenous, intraperitoneal, oral) administrations. One strategy to improve the delivery of antioxidants to the brain involves the use of the so-called nose-to-brain route, with the administration of the antioxidant in specific nasal formulations and its passage to the central nervous system (CNS) mainly through the olfactory nerve way. In the current literature, many examples show encouraging results in studies carried out in cell cultures and in animal models about the potential neuroprotective effects of antioxidants when administered through the nose. This review concerns the nose-to-brain route for the brain targeting of antioxidants as a potential tool for the therapy of neurological diseases.

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