4 edition of The Role of Oxidative Stress in Neuronal Death found in the catalog.
by Landes Bioscience
Written in English
Medical Intelligence Unit Series
|The Physical Object|
|Number of Pages||203|
Oxidative stress and the shape of cell death. Loss of glutathione and oxidative damage have been suggested to constitute early, possibly signaling events in apoptotic cell death [[3, 4]].In thymocytes, a decrease of GSH and disruption of the mitochondrial transmembrane potential preceded the onset of apoptosis [[5, 6]].A rapid loss of GSH was found recently in IL3 withdrawal‐induced Cited by: Oxidative damage to major cellular molecules is seen in a number of disease states that are either acute or chronic and it is apparent that without eliciting compensations that restore redox balance, cells will rapidly succumb to death. Indeed, although oxidative stress is a prominent feature in Alzheimer disease, few vulnerable neurons show clear signs of apoptosis, suggesting that the level of oxidative stress Cited by:
Oxidative stress induces numerous signaling pathways, including DNA damage response (DDR), associated with the breast cancer type 1 susceptibility protein (BRCA1) protein, known to date from numerous reports in the cancer field. In this Viewpoint, we discuss the latest discoveries related to the role of BRCA1 in the death of neurons in : M. Wezyk, C. Zekanowski. Oxidative damage plays a key role in the development of Alzheimer disease. In this Review, Butterfield and Halliwell discuss how this damage relates Cited by:
This article is from International Journal of Molecular Sciences, volume AbstractThe primary physiological function of mitochondria is to generate adenosine. We investigated the role of mitochondria in oxidative stress-induced necrotic neuronal cell death in a neuroblastoma cell line and a mouse model of middle cerebral artery occlusion. The exogenous administration of hydrogen peroxide was used to study the role of oxidative stress on neuronal cell survival and mitochondrial function in vitro.
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The Role of Oxidative Stress in Neuronal Death Paperback – Ma by Irene Ceballos-Picot (Author) See all 4 formats and editions Hide other formats and editions. Price New from Used from Hardcover "Please retry" $ — $ Author: Irene Ceballos-Picot. This is the first book to point out the role of oxidative stress as a causal agent in neurodegenerative diseases (e.g.
Alzheimer's disease).Brand: Springer-Verlag Berlin Heidelberg. The Role of Oxidative Stress The Role of Oxidative Stress in Neuronal Death book Neuronal Death. Authors (view affiliations) Irène Ceballos-Picot; Book. 15 Citations; Oxidative Stress in Neuronal Death and Apoptosis.
Oxidative Stress, Cerebral Aging and Longevity. Irène Ceballos-Picot. Pages Oxidative Stress in. The Role of Oxidative Stress in Neuronal Death.
[Irène Ceballos-Picot] -- This book examines current knowledge and recent advances in the study of fundamental processes involved in neuronal death, particularly oxidative stress as a causal agent or risk factor. This book examines current knowledge and recent advances of fundamental processes involved in neuronal death, particularly oxida- tive stress as a causal, or at least an ancillary, factor in neuronal death.
This book also presents an up-to-date account of the current state of knowledge about of oxidative stress in neuronal apoptosis and its role in the neuropathogenesis of age-related Author: Irene Ceballos-Picot.
Biology of Oxidative Stress Oxidative Stress in Neuronal Death and Apoptosis Oxidative Stress, Cerebral Aging and Longevity Oxidative Stress in Alzheimer's Disease Oxidative Stress in Down's Syndrome Oxidative Stress in Amyotrophic Lateral Sclerosis Oxidative Stress in Parkinson's Disease Conclusions.
Series. Oxidative stress, resulting from a deregulation of the balance of pro-oxidants/antioxidants, results in a number of phenomena from activation of signaling mechanisms, deregulation of Ca 2+ homeostasis, alterations of mitochondrial structure and function and alterations in cellular structure to alterations in gene expression, all of which contribute to or play a critical role in neuronal by: 5.
Oxidative stress has been implicated in neuronal cell death in a variety of neurologic disorders. Oxidative stress influences the oxidation states of several proteins in neuronal cells involved in.
Based on the above data, we propose that autophagosome processing is impaired in the cortex after CA-ROSC, resulting in the accumulation of autophagosomes and ubiquitinated proteins, which is related to neuronal cell death.
Inhibiting the generation of oxidative stress can restore the autophagic fluxCited by: 3. The Role of Oxidative Stress in Neuronal Death Neuroscience Intelligence Unit: : Irene Ceballos-Picot: BooksAuthor: Irene Ceballos-Picot. Oxidative stress mediated neurodegeneration can execute through bioenergetic failure, depletion of antioxidant defences, bio molecular damage, microtubular disruption, ion channel activation, demyelination, neuroinflammation, mitophagy impairment and Cited by: As mitochondrial dysfunction with excessive oxidative stress may play a crucial role in ischemic cascades, counteracting this detrimental effect through better understanding the neuronal damage resulting from apoptotic or necrotic cell death should have the perspective in treating ROS-related disorders such as ischemic by: Download The Role of Oxidative Stress in Neuronal Death PDF Full Ebook.
Download The Role of Oxidative Stress in Neuronal Death PDF Full Ebook. Report. Browse more videos. Playing next. Read An Introduction to Vitamins Minerals and Oxidative Stress: The Role of Micronutrients Medicine Book Review: Oxidative Stress in Cancer, AIDS.
Oxidative stress and diabetes on neuronal function and metabolism: The neuroprotective role of insulin: Medicine & Health Science Books @ hor: Ana Duarte.
Oxidative stress has the potential to damage proteins, lipids, or DNA, but whether this damage is a mediator of neuronal death or a consequence of oxidative death is unclear.
PGC1-α is also involved in mitochondrial biogenesis that is vital for cell survival. Experimental evidence supports the roles of mitochondrial dysfunction and oxidative stress as determinants of neuronal death as well as endogenous protective mechanisms after by: A major consequence of oxidative/nitrosative stress is damage to nucleic acid bases, lipids, and proteins, which can severely compromise cell health and viability or induce a variety of cellular responses through generation of secondary reactive species, ultimately leading to cell death by necrosis or apoptosis .Author: Hiba A.
Awooda. Oxidative stress has been shown to decrease the activity of histone deacetylases 1–10 (66). This change in deacetylase activity could lead to a global inactivation of transcriptional repressors, leading to activation of numerous genes (including cell cycle–inducing genes) and subsequent cell by: Although the exact neuronal lesion mechanisms underlying neurodegenerative disorders, including dementia, are not yet known, most recent studies suggest oxidative stress and mitochondrial dynamics’ role in the ive: Literature review on the role of oxidative stress’ role in aging and s: Literature Author: Joana Teixeira, Marcelo Feio, Maria Luísa Figueira.
Free radicals and oxidative stress‐induced neuronal cell death have been implicated in a variety of neurological disorders. Therefore, neuroprotection is of primary interest in basic and preclinical Cited by:.
Early changes in cerebral oxidative stress and apoptotic neuronal injury after various flows for selective cerebral perfusion in piglets 18 May | Perfusion, Vol. 27, No. 5 A novel Drosophila SOD2 mutant demonstrates a role for mitochondrial ROS in neurodevelopment and diseaseCited by: Abstract.
Reactive oxygen species (ROS) cause death of cerebellar granule neurons. Here, a min pulse of H 2 O 2 ( μ m) induced an active process of neuronal death distinct from ive stress activated a caspase-independent but calpain-dependent decline of calcium/calmodulin-dependent protein kinase IV and cAMP- responsive element-binding protein (CREB).The mechanisms that account for this selective neuronal death are multifaceted in nature and several lines of evidence suggest that mitochondrial dysfunction, overproduction of reactive oxygen species (ROS) and oxidative stress (an imbalance between pro-oxidant and antioxidant systems resulting in oxidative damage to proteins, lipids and DNA Cited by: