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 Immunocytochemical localization of catalase in the central nervous system of the rat.

1995 ◽  
Vol 43 (12) ◽  
pp. 1253-1267 ◽  
Author(s):  
S Moreno ◽  
E Mugnaini ◽  
M P Cerù
Keyword(s):  
Reactive Oxygen Species ◽  
Central Nervous System ◽  
Nervous System ◽  
Reperfusion Injury ◽  
Brain Aging ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Ependymal Cells ◽  
Oxygen Species

Catalase is a marker for peroxisomes, which are ubiquitous cytoplasmic organelles. Although the distribution and features of peroxisomes are well known in liver and kidney, these organelles have been rarely studied in neural tissues. Catalase is an important scavenging enzyme against reactive oxygen species, as it removes H2O2 produced during metabolic processes. Reactive oxygen species are involved in a number of brain lesions and in brain aging. We investigated the distribution of catalase in rat central nervous system by means of a newly developed immunocytochemical procedure for signal enhancement, using an affinity-purified polyclonal antiserum. The data show that catalase immunoreactivity is present in all neural cells, both neuronal and glial, albeit at different concentrations. Among glial cells, ependymal cells and tanycytes of the third ventricle and the median eminence show the most intense immunoreaction; positivity is also found in oligodendrocytes and astrocytes. In general, neurons in the brainstem are relatively more immunoreactive than those in the forebrain although, within these respective brain regions, there are areas with low and high staining intensity. Moreover, within the same area, certain types of neuron appear more immunoreactive than others. The cell bodies in the septal nuclei, pallidum, reticular thalamic nucleus, mesencephalic nucleus of the trigeminal nerve, Deiter's nucleus, locus ceruleus, cranial and spinal motor nuclei, and the Golgi cells of the cerebellar cortex are among the most densely stained neurons. Catalase immunoreactivity of the cell bodies, which presumably is proportional to catalase content, appears to be only partially correlated with cell size or type of neurotransmitter used in the nerve endings; it is likely that other unknown parameters regulate the abundance of the enzyme. In many cases, highly immunoreactive cells correspond to neurons known to be resistant to ischemia-reperfusion injury, whereas weakly stained cells correspond to neurons that are more susceptible to ischemic damage. The amount of catalase may be critical for a protective effect against oxidative stress under pathological conditions, such as ischemia-reperfusion injury.

scholarly journals Microglia and Macrophages in the Pathological Central and Peripheral Nervous Systems

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 2132 ◽  
Author(s):  
Naoki Abe ◽  
Tasuku Nishihara ◽  
Toshihiro Yorozuya ◽  
Junya Tanaka
Keyword(s):  
Reactive Oxygen Species ◽  
Central Nervous System ◽  
Nervous System ◽  
Oxidative Phosphorylation ◽  
Oxygen Species ◽  
Neuroprotective Effects ◽  
Inflammatory Activation ◽  
The Central Nervous System ◽  
Anti Inflammatory ◽  
Inflammatory Phenotypes

Microglia, the immunocompetent cells in the central nervous system (CNS), have long been studied as pathologically deteriorating players in various CNS diseases. However, microglia exert ameliorating neuroprotective effects, which prompted us to reconsider their roles in CNS and peripheral nervous system (PNS) pathophysiology. Moreover, recent findings showed that microglia play critical roles even in the healthy CNS. The microglial functions that normally contribute to the maintenance of homeostasis in the CNS are modified by other cells, such as astrocytes and infiltrated myeloid cells; thus, the microglial actions on neurons are extremely complex. For a deeper understanding of the pathophysiology of various diseases, including those of the PNS, it is important to understand microglial functioning. In this review, we discuss both the favorable and unfavorable roles of microglia in neuronal survival in various CNS and PNS disorders. We also discuss the roles of blood-borne macrophages in the pathogenesis of CNS and PNS injuries because they cooperatively modify the pathological processes of resident microglia. Finally, metabolic changes in glycolysis and oxidative phosphorylation, with special reference to the pro-/anti-inflammatory activation of microglia, are intensively addressed, because they are profoundly correlated with the generation of reactive oxygen species and changes in pro-/anti-inflammatory phenotypes.

Oxidative Stress and Accelerated Aging in Neurodegenerative and Neuropsychiatric Disorder

2019 ◽  
Vol 24 (40) ◽  
pp. 4711-4725 ◽  
Author(s):  
Ridhima Wadhwa ◽  
Riya Gupta ◽  
Pawan K. Maurya
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Oxidative Damage ◽  
Neurodegenerative Diseases ◽  
Bipolar Depression ◽  
Environmental Pollutants ◽  
X Rays ◽  
Neuropsychiatric Diseases ◽  
The Central Nervous System

Background: Neurodegenerative diseases are becoming more and more common in today’s world. As people are continuously being exposed to exogenous factors like UV radiations, gamma rays, X-Rays, environmental pollutants and heavy metals, the cases of increased oxidative damage are increasing. Even though some amount of oxidative damage occurs in all metabolic reactions but their increase from the normal level in organisms causes neurodegenerative diseases. These neurodegenerative disorders like Alzeimers, Parkinsons disease and neuropsychiatric disorders such as schizophrenia, bipolar, depression are caused due to the decline in physiological and psychological functions caused by ROS and RNS. These ROS and RNS are formed as the result of excess oxidative damage in the system. Methods: The following article goes into detail explaining all the effects caused by excess oxidative damage like ROS/RNS formation and telomere shortening. Further, it explains the pathways of neurodegenerative diseases and neuropsychiatric diseases. This article also sheds light on the effective treatments of such disorders by changing lifestyle and activating antioxidant pathways. Conclusion: It is clear that neurodegenerative diseases are caused due to excess oxidative stress and alter the functioning of the central nervous system. The central nervous system undergoes neurodegenerative or neuropsychiatric changes.

LONG TERM PRODUCTION OF REACTIVE OXYGEN SPECIES DURING PERINATAL ASPHYXIA IN THE RAT CENTRAL NERVOUS SYSTEM: EFFECTS OF HYPOTHERMIA

2003 ◽  
Vol 113 (5) ◽  
pp. 641-654 ◽  
Author(s):  
FRANCISCO CAPANI ◽  
CÉSAR FABIÁN LOIDL ◽  
LIDIA LEONOR PIEHL ◽  
GRACIELA FACORRO ◽  
TOMÁS DE PAOLI ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Central Nervous System ◽  
Nervous System ◽  
Perinatal Asphyxia ◽  
Reactive Oxygen ◽  
Oxygen Species

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.

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