scholarly journals Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Marisela Méndez-Armenta ◽  
Concepción Nava-Ruíz ◽  
Daniel Juárez-Rebollar ◽  
Erika Rodríguez-Martínez ◽  
Petra Yescas Gómez
Keyword(s):  
Oxidative Stress ◽  
Neuronal Death ◽  
Neurological Disorders ◽  
Neuronal Apoptosis ◽  
Experimental Models ◽  
State Failure ◽  
Radical Production ◽  
Induction Of Apoptosis ◽  
Models Of Epilepsy

Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy.

scholarly journals The Role of NADPH Oxidase in Neuronal Death and Neurogenesis after Acute Neurological Disorders

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 739
Author(s):  
Song-Hee Lee ◽  
Min-Woo Lee ◽  
Dong-Gyun Ko ◽  
Bo-Young Choi ◽  
Sang-Won Suh
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Neuronal Death ◽  
Neurological Disorders ◽  
Reactive Oxygen ◽  
Neuronal Injury ◽  
Oxygen Species ◽  
Comprehensive Overview

Oxidative stress is a well-known common pathological process involved in mediating acute neurological injuries, such as stroke, traumatic brain injury, epilepsy, and hypoglycemia-related neuronal injury. However, effective therapeutic measures aimed at scavenging free reactive oxygen species have shown little success in clinical trials. Recent studies have revealed that NADPH oxidase, a membrane-bound enzyme complex that catalyzes the production of a superoxide free radical, is one of the major sources of cellular reactive oxygen species in acute neurological disorders. Furthermore, several studies, including our previous ones, have shown that the inhibition of NADPH oxidase can reduce subsequent neuronal injury in neurological disease. Moreover, maintaining appropriate levels of NADPH oxidase has also been shown to be associated with proper neurogenesis after neuronal injury. This review aims to present a comprehensive overview of the role of NADPH oxidase in neuronal death and neurogenesis in multiple acute neurological disorders and to explore potential pharmacological strategies targeting the NADPH-related oxidative stress pathways.

scholarly journals Protective Role of Glutathione in the Hippocampus after Brain Ischemia

2021 ◽  
Vol 22 (15) ◽  
pp. 7765
Author(s):  
Youichirou Higashi ◽  
Takaaki Aratake ◽  
Takahiro Shimizu ◽  
Shogo Shimizu ◽  
Motoaki Saito
Keyword(s):  
Oxidative Stress ◽  
Neuronal Death ◽  
Excitatory Amino Acid ◽  
Ischemia Reperfusion ◽  
Thiol Group ◽  
Protective Role ◽  
Key Factor ◽  
Rate Limiting ◽  
Cysteine Uptake

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.

scholarly journals Vitamin E Analogues Inhibit Angiogenesis by Selective Induction of Apoptosis in Proliferating Endothelial Cells: The Role of Oxidative Stress

2007 ◽  
Vol 67 (24) ◽  
pp. 11906-11913 ◽  
Author(s):  
L.-F. Dong ◽  
E. Swettenham ◽  
J. Eliasson ◽  
X.-F. Wang ◽  
M. Gold ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vitamin E ◽  
Induction Of Apoptosis

Role of Vitamins in Neurodegenerative Diseases: A Review

2021 ◽  
Vol 20 ◽  
Author(s):  
Ravi Ranjan Kumar ◽  
Lovekesh Singh ◽  
Amandeep Thakur ◽  
Shamsher Singh ◽  
Bhupinder Kumar
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Vitamin D ◽  
Vitamin C ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Vitamin D Deficiency ◽  
Neurological Disorders ◽  
The Brain

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity. Methods: In this review, we have compiled various reports collected from PubMed, Scholar Google, Research gate, and Science direct. The findings were evaluated, compiled, and represented in this manuscript. Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer’s disease, Parkinson’s disease, Huntington's disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer’s disease, there is a lack of vitamin-B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson’s disease, vitamin-D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, Vitamin-C and Vitamin-D deficiency causes demyelination of neurons. In Huntington's disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. Vitamin B5 deficiency in Huntington's disease disrupts the synthesis of acetylcholine and hormones in the brain.

scholarly journals Modulation of Oxidative Stress by Ozone Therapy in the Prevention and Treatment of Chemotherapy-Induced Toxicity: Review and Prospects

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 588 ◽  
Author(s):  
Bernardino Clavo ◽  
Francisco Rodríguez-Esparragón ◽  
Delvys Rodríguez-Abreu ◽  
Gregorio Martínez-Sánchez ◽  
Pedro Llontop ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Potential Role ◽  
Antioxidant Response ◽  
Experimental Models ◽  
Ozone Therapy ◽  
Oxidative Stress Parameters ◽  
Randomized Controlled ◽  
Causes Of Mortality

(1) Background: Cancer is one of the leading causes of mortality worldwide. Radiotherapy and chemotherapy attempt to kill tumor cells by different mechanisms mediated by an intracellular increase of free radicals. However, free radicals can also increase in healthy cells and lead to oxidative stress, resulting in further damage to healthy tissues. Approaches to prevent or treat many of these side effects are limited. Ozone therapy can induce a controlled oxidative stress able to stimulate an adaptive antioxidant response in healthy tissue. This review describes the studies using ozone therapy to prevent and/or treat chemotherapy-induced toxicity, and how its effect is linked to a modification of free radicals and antioxidants. (2) Methods: This review encompasses a total of 13 peer-reviewed original articles (most of them with assessment of oxidative stress parameters) and some related works. It is mainly focused on four drugs: Cisplatin, Methotrexate, Doxorubicin, and Bleomycin. (3) Results: In experimental models and the few existing clinical studies, modulation of free radicals and antioxidants by ozone therapy was associated with decreased chemotherapy-induced toxicity. (4) Conclusions: The potential role of ozone therapy in the management of chemotherapy-induced toxicity merits further research. Randomized controlled trials are ongoing.

Essential oils in experimental models of neuropsychiatric disorders: A review

2021 ◽  
Vol 19 ◽  
Author(s):  
Luciana Cristina B. Fernandes ◽  
Ianara Mendonça Costa ◽  
Marco Aurelio M. Freire ◽  
Francisca Overlânia V. Lima ◽  
Francisca Idalina Neta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Systematic Review ◽  
Cerebral Ischemia ◽  
Essential Oils ◽  
Neurological Disorders ◽  
Biological Effects ◽  
Neuroprotective Effect ◽  
Experimental Models ◽  
Sensory Loss ◽  
Cochrane Library

Background: Neural cells undergo functional or sensory loss due to neurological disorders. In addition to environmental or genetic factors, oxidative stress is a major contributor to neurodegeneration. In this context, there has been a growing interest in investigating the effects of essential oils (EOs) in recent years, especially in the treatment of neuropathologies. The chemical and biological effects of EOs have led to important treatment tools for the management of various neurological disorders. Objective: In the present study we performed a systematic review that sought to comprehend the neuroprotective effects of different EOs. Method: This work is a systematic review where an electronic search was performed on PubMed, Science direct, Cochrane Library and SciELO (Scientific Electronic Library Online) databases, covering the last 10 years, using “Essential oil” and “Neuroprotective effect” as reference terms. Results: A total of 9 articles were identified, in which the efficacy of EOs was described in experimental models of anxiety, dementia, oxidative stress, cerebral ischemia, Alzheimer’s disease and oxidative toxicity. Conclusion: EOs from different species of medicinal plants have shown positive responses in neurological disorders such as anxiety, dementia, oxidative stress, cerebral ischemia and oxidative toxicity. Thus, EOs emerges with the potential to be used as alternative agents in the treatment of neurological disorders.

scholarly journals FructationIn Vivo: Detrimental and Protective Effects of Fructose

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
H. M. Semchyshyn
Keyword(s):  
Oxidative Stress ◽  
Side Effects ◽  
Experimental Models ◽  
Oxygen Species ◽  
Protective Effects ◽  
Compelling Evidence ◽  
Animal Tissues

There is compelling evidence that long-term intake of excessive fructose can have deleterious side effects in different experimental models. However, the role of fructosein vivoremains controversial, since acute temporary application of fructose is found to protect yeast as well as animal tissues against exogenous oxidative stress. This review suggests the involvement of reactive carbonyl and oxygen species in both the cytotoxic and defensive effects of fructose. Potential mechanisms of the generation of reactive species by fructose in the nonenzymatic reactions, their implication in the detrimental and protective effects of fructose are discussed.

scholarly journals Antioxidant therapies in traumatic brain injury: a review

2017 ◽  
Vol 31 (3) ◽  
pp. 319-334
Author(s):  
Hector Rolando Romero-Rivera ◽  
Marticela Cabeza-Morales ◽  
Enrique Soto-Zarate ◽  
Guru Dutta Satyarthee ◽  
Huber Padilla-Zambrano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Death ◽  
Good Alternative ◽  
Secondary Injury ◽  
Injury Management ◽  
Definitive Therapy ◽  
Unconventional Therapies

Abstract Oxidative stress constitute one of the commonest mechanism of the secondary injury contributing to neuronal death in traumatic brain injury cases. The oxidative stress induced secondary injury blockade may be considered as to be a good alternative to improve the outcome of traumatic brain injury (TBI) treatment. Due to absence of definitive therapy of traumatic brain injury has forced researcher to utilize unconventional therapies and its roles investigated in the improvement of management and outcome in recent year. Antioxidant therapies are proven effective in many preclinical studies and encouraging results and the role of antioxidant mediaction may act as further advancement in the traumatic brain injury management it may represent aonr of newer moadlaity in neurosurgical aramamentorium, this kind of therapy could be a good alternative or adjuct to the previously established neuroprotection agents in TBI.

scholarly journals Ceramides in Alzheimer’s Disease: Key Mediators of Neuronal Apoptosis Induced by Oxidative Stress and AβAccumulation

2015 ◽  
Vol 2015 ◽  
pp. 1-17 ◽  
Author(s):  
Maja Jazvinšćak Jembrek ◽  
Patrick R. Hof ◽  
Goran Šimić
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Apoptosis ◽  
Neurodegenerative Disorder ◽  
Neuronal Degeneration ◽  
Sphingolipid Metabolism ◽  
Cytochrome C Release ◽  
Biochemical Alterations

Alzheimer’s disease (AD), the most common chronic and progressive neurodegenerative disorder, is characterized by extracellular deposits of amyloidβ-peptides (Aβ) and intracellular deposits of hyperphosphorylated tau (phospho-tau) protein. Ceramides, the major molecules of sphingolipid metabolism and lipid second messengers, have been associated with AD progression and pathology via Aβgeneration. Enhanced levels of ceramides directly increase Aβthrough stabilization ofβ-secretase, the key enzyme in the amyloidogenic processing of Aβprecursor protein (APP). As a positive feedback loop, the generated oligomeric and fibrillar Aβinduces a further increase in ceramide levels by activating sphingomyelinases that catalyze the catabolic breakdown of sphingomyelin to ceramide. Evidence also supports important role of ceramides in neuronal apoptosis. Ceramides may initiate a cascade of biochemical alterations, which ultimately leads to neuronal death by diverse mechanisms, including depolarization and permeabilization of mitochondria, increased production of reactive oxygen species (ROS), cytochrome c release, Bcl-2 depletion, and caspase-3 activation, mainly by modulating intracellular signalling, particularly along the pathways related to Akt/PKB kinase and mitogen-activated protein kinases (MAPKs). This review summarizes recent findings related to the role of ceramides in oxidative stress-driven neuronal apoptosis and interplay with Aβin the cascade of events ending in neuronal degeneration.

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