Bioenergetics in Oxidative Damage in Neurodegenerative Diseases

1996 ◽  
pp. 171-179 ◽  
Author(s):  
M. Flint Beal
Keyword(s):  
Oxidative Damage ◽  
Neurodegenerative Diseases

scholarly journals Protein Targets of Oxidative Damage in Human Neurodegenerative Diseases with Abnormal Protein Aggregates

2010 ◽  
Vol 20 (2) ◽  
pp. 281-297 ◽  
Author(s):  
Anna Martínez ◽  
Manuel Portero-Otin ◽  
Reinald Pamplona ◽  
Isidre Ferrer
Keyword(s):  
Oxidative Damage ◽  
Neurodegenerative Diseases ◽  
Protein Aggregates ◽  
Protein Targets ◽  
Abnormal Protein

Hallmarks of protein oxidative damage in neurodegenerative diseases: focus on Alzheimer’s disease

Amino Acids ◽  
2007 ◽  
Vol 32 (4) ◽  
pp. 553-559 ◽  
Author(s):  
M. C. Polidori ◽  
H. R. Griffiths ◽  
E. Mariani ◽  
P. Mecocci
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oxidative Damage ◽  
Neurodegenerative Diseases

scholarly journals Interference with ubiquitination causes oxidative damage and increased protein nitration: implications for neurodegenerative diseases

2004 ◽  
Vol 90 (2) ◽  
pp. 422-430 ◽  
Author(s):  
Dong-Hoon Hyun ◽  
Douglas A. Gray ◽  
Barry Halliwell ◽  
Peter Jenner
Keyword(s):  
Oxidative Damage ◽  
Neurodegenerative Diseases ◽  
Protein Nitration

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.

Oxidative Damage in Neurodegenerative Diseases

1997 ◽  
Vol 3 (1) ◽  
pp. 21-27 ◽  
Author(s):  
M. Flint Beal
Keyword(s):  
Nitric Oxide ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Superoxide Dismutase ◽  
Oxidative Damage ◽  
Neurodegenerative Diseases ◽  
Protein Nitration ◽  
Cuzn Superoxide Dismutase ◽  
Radical Generation ◽  
Familial Als

Increasing evidence has implicated oxidative damage in the pathogenesis of neurodegenerative diseases. The major source of free radicals in the cell is the mitochondria. Peroxynitrite is formed by the reaction of superoxide with nitric oxide, and it produces both oxidative damage and protein nitration. Mutations in CuZn superoxide dismutase associated with familial ALS may result in increased −OH radical generation or in increased reactivity with peroxynitrite to nitrate proteins. There is evidence for increased oxidative damage in Alzheimer's disease and Parkinson's disease in neurons undergoing neurodegenerative changes. A role for oxidative damage in Parkinson's disease toxicity and in Huntington's disease is supported by studies in animal models. Improved antioxidant therapies may prove useful in slowing or halting the progression of neurodegenerative diseases.

scholarly journals Protective effect of serotonin derivatives on glucose-induced damage in PC12 rat pheochromocytoma cells

2009 ◽  
Vol 103 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Rosaria Piga ◽  
Yuji Naito ◽  
Satoshi Kokura ◽  
Osamu Handa ◽  
Toshikazu Yoshikawa
Keyword(s):  
Oxidative Damage ◽  
Neurodegenerative Diseases ◽  
Protective Effect ◽  
Neuronal Damage ◽  
Present Report ◽  
Radical Scavenging ◽  
Antioxidant Property ◽  
Safflower Seed ◽  
Dependent Manner ◽  
Serotonin Derivatives

Oxidative damage is believed to be associated with ageing, cancer and several degenerative diseases. Previous reports have shown that safflower-seed extract and its major antioxidant constituents, serotonin hydroxycinnamic amides, possess a powerful free radical-scavenging and antioxidative activity, paying particular attention to atherosclerotic reactive oxygen species (ROS)-related dysfunctions. In the present report, we examined a still unknown cell-based mechanism of serotonin derivatives against ROS-related neuronal damage, phenomena that represent a crucial event in neurodegenerative diseases. Serotonin derivatives N-(p-coumaroyl)serotonin and N-feruloylserotonin exerted a protective effect on high glucose-induced cell death, inhibited the activation of caspase-3 which represents the last and crucial step within the cascade of events leading to apoptosis, and inhibited the overproduction of the mitochondrial superoxide, which represents the most dangerous radical produced by hyperglycaemia, by acting as scavengers of the superoxide radical. In addition, serotonin derivative concentration inside the cells and inside the mitochondria was increased in a time-dependent manner. Since recent studies support the assertion that mitochondrial dysfunctions related to oxidative damage are the major contributors to neurodegenerative diseases, these preliminary cell-based results identify a mitochondria-targeted antioxidant property of serotonin derivatives that could represent a novel therapeutic approach against the neuronal disorders and complications related to ROS.

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