2 edition of effect of free radicals in neuronal apoptosis found in the catalog.
effect of free radicals in neuronal apoptosis
Thesis (Ph.D.) - University of Warwick, 2000.
|The Physical Object|
|Number of Pages||184|
BrightFocus Foundation Gateway Center Drive Clarksburg, MD See previous address. Phone: Fax: () E-mail: [email protected] Neural cell death has a pivotal role in both the development and pathophysiology of the nervous system. Two distinct modes of cell death—necrosis and apoptosis—are involved in pathological neuronal loss, but apoptosis alone is the mechanism of programmed cell death during development. All cells will undergo apoptosis in the absence of survival signals, usually peptide growth factors Cited by:
During these processes, large amounts of free radicals (reactive oxygen and nitrogen species) were produced,. Excessive production of free radicals (reactive oxygen and nitrogen species) causes an imbalance between pro-oxidants and antioxidants and damages biomolecules, such as proteins, lipids, and nucleic by: Free radical-triggered and age-accumulated oxidation may modify the program controlling motor neuron death, thereby initiating apoptosis of motor neurons in young adults.", keywords = "Amyotrophic lateral sclerosis, Cu,Zn superoxide dismutase, Free radicals, Glutamate toxicity, Motor neuron degeneration, Oxidative damage, Programmed neuron death",Cited by:
Effect of Free Radicals on the Body: Oxidative Stress. Once free radicals are generated, whether through exposure to a carcinogen or doing the normal processes of body metabolism, they are free to do damage. The availability of free radicals creates what is known as oxidative stress in the body. The reason it is named oxidative stress is that. The present study shows a detrimental effect of the radical scavenger PBN in experimental S. pneumoniae meningitis, leading to an increase in hippocampal apoptosis and, in consequence, to impaired learning function. This is the first report to relate the severity of hippocampal apoptosis as a consequence of bacterial meningitis to reduced Cited by:
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Free radicals play a crucial role in brain ischemic injury by exacerbating membrane damage through peroxidation of unsaturated fatty acids of cell membrane, leading to neuronal death and brain edema. Free radicals have been implicated in stroke pathophysiology as pivotal contributors to cell injury.
Edaravone (3‐methyl‐1‐phenyl‐2‐pyrazolin‐5‐one) is a novel potent free radical scavenger that has Cited by: Apoptosis is an active process of cell destruction, characterized by cell shrinkage, chromatin aggregation with extensive genomic fragmentation, and nuclear pyknosis. In contrast, necrosis is characterized by passive cell swelling, intense mitochondrial damage with rapid energy loss, and generalized disruption of internal by: Effects of free radicals on cell proliferation and apoptosis Gener ation of FR has been proposed to stimulate cellular proliferation and deletion by apoptosis [5, 14, 15], but there is no single.
Xanthine oxidase is a free radical-producing substance. Thus, our results indicate that SHRSP/Izm neurons are damaged by ischemia and by oxygen radicals generated after reperfusion. Vitamin E reacts with the oxygen radicals, thereby inhibiting apoptosis and by: 1.
Effects of Sofren injection combined with oxygen free radical scavenger on neural function and apoptosis in patients with acute cerebral infarction. Jian-Ping Feng. Department of Neurological Rehabilitation, Xi’an Union Hospital in Shaanxi Province, Xi’an, Shaanxi Province,China.
Journal of Hainan Medical University. Aβ increased free radical production and lipid peroxidation in PC12 nerve cells, leading to increased 4-hydroxynonenal (HNE) production and modification of specific mitochondrial target proteins, apoptosis and cell by: Free Radical Induced Apoptosis Pathway (Concept Id: C) Oxidative stress is one factor that can trigger programmed cell death.
Activated neutrophils responding to inflammatory stimulation produce reactive oxygen species like superoxide free radicals to kill invading bacteria, but these reactive oxygen species can also attack endothelial cells lining the vascular wall and trigger apoptosis. Free radicals are produced either endogenously (by metabolism and antioxidant system of the body) or exogenously (by environmental sources) by imbalance between antioxidant and prooxidant in the body.
Free radicals, particularly ROS have been proposed as common mediators for apoptosis. Recent studies have demonstrated that the mode of cell death depends on the severity of the oxidative damage. Free radicals generated during cerebral ischaemia (a irst wave within minutes followed by a second wave shortly thereafter) participate in the cascade of events generating neuronal damage, which.
Free radicals generated during SAH results in neuronal damage by promoting lipid peroxidation, protein breakdown, and DNA damage, these effects in turn lead to cellular apoptosis, and BBB permeability. Previous studies have indicated that ROS contributes to the disruption of BBB by disturbing tight junction by: Free radicals destroy the structure of the cell membrane structure and attack DNA, fracturing it and increasing the rate of apoptosis.
They are considered to be closely correlated with. 1 Free radicals and antioxidants in brain pathophysiology --Role of free radicals in the brain in health and disease in relation to synaptic plasticity / John Smythies --Neuromodulatory effects of nitric oxide in pain perception / Adalberto Merighi --Ischemic and metabolic stress-induced apoptosis / James David Adams --Nitrogen radicals in.
The mutations of the Cu,Zn superoxide dismutase (Cu,Zn-SOD) gene observed in amyotrophic lateral sclerosis (ALS) patients suggest that free radicals play a role in this fatal disease. Free radicals trigger oxidative damage to proteins, membrane lipids, and DNA, thereby destroying neurons.
Mutations of the SOD gene may reduce its superoxide dismutase activity, thereby elevating free radical Cited by: Neuronal apoptosis after excitotoxic insult involves Ca 2+ overload, p38 MAPK activation, release of cytochrome c from mitochondria, activation of caspases, free-radical.
Amyloid-β might induce apoptosis 61 by interacting with neuronal receptors, including the receptor for advanced glycation endproducts (RAGE), which can mediate free-radical product Cited by: Free radical theory of apoptosis and metamorphosis Masayasu Inoue 1, Eisuke F.
Sato 1, Manabu Nishikawa, Keiichi Hiramoto, Akihiko Kashiwagi 2, Kozo Utsumi 3 Effect of Ca 2+ on mitochondria-dependent apoptosis In the presence of respiratory substrates and P i, Ca 2+ also induces MPT.
Increased free radicals and consequent increase in the protein oxidative damages might be playing a significant role in the apoptotic neuronal death leading to the development of neuronal toxicity in long-term aspartame by: ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca 2+ overload and excitotoxicity.
These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the by: Polyphenols are natural substances with variable phenolic structures and are elevated in vegetables, fruits, grains, bark, roots, tea, and wine.
There are over polyphenolic structures identified in plants, but edible plants contain only several hundred polyphenolic structures.
In addition to their well-known antioxidant effects, select polyphenols also have insulin-potentiating, anti Cited by:. Methamphetamine (METH) is an illegal psychoactive substance that is abused worldwide, and repeated exposure to METH could form mass free radicals and induce neuronal apoptosis.
It has been reported that free radicals generated by METH treatment can oxidize DNA and hence produce strand breaks, but whether oxidative DNA damage is involved in the neurotoxicity Author: Qin Ru, Qi Xiong, Xiang Tian, Lin Chen, Mei Zhou, Yi Li, Chaoying Li.Toxicity of free radicals contributes to proteins and DNA injury, inflammation, tissue damage and subsequent cellular apoptosis.
Antioxidants are now being looked upon as persuasive therapeutic against solemn neuronal loss, as they have capability to combat by neutralizing free radicals.We examined the neuroprotective effects of Choto-san using an experimental cerebral ischemia model (i.e., a rat cardiac arrest model).
We also investigated the ability of Choto-san to eliminate or inhibit the activity of free radicals. It was found that Choto-san significantly prevents delayed neuronal cell death after ischemic by: 6.