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Books on the topic 'Mitochondrial oxidative stress'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Saavedra-Molina, Alfredo. Mitochondrial dysfunctions related to oxidative stress. Nova Science Publishers, 2010.

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2

E, Gibson Gary, Ratan Rajiv R, and Beal M. Flint, eds. Mitochondria and oxidative stress in neurodegenerative disorders. Wiley-Blackwell, 2008.

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3

Flint, Beal M., Howell Neil 1946-, and Bodis-Wollner Ivan 1937-, eds. Mitochondria and free radicals in neurodegenerative diseases. Wiley-Liss, 1997.

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4

Mitochondria in health and disease. Dekker, 2005.

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5

Berdanier, Carolyn D. Mitochondria in Health and Disease. Taylor & Francis Group, 2019.

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6

Berdanier, Carolyn D. Mitochondria in Health and Disease. Taylor & Francis Group, 2005.

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7

Berdanier, Carolyn D. Mitochondria in Health and Disease. Taylor & Francis Group, 2005.

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8

Knott, Andrew B., and Ella Bossy-Wetzel. Mitochondrial Changes and Bioenergetics in Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0012.

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Mitochondria are dynamic organelles that are of critical importance for cellular survival and health. Because mitochondria play central roles in energy production and synaptic maintenance, neurons are believed to be particularly vulnerable to mitochondrial dysfunction. The discovery that genetic mutations in genes coding for mitochondrial proteins cause neurodegenerative conditions further hinted at the likelihood that mitochondrial dysfunction is a key pathway of neurodegeneration. Indeed, a wealth of research has identified mitochondrial dysfunction as an early and shared event of all common

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9

Neurodegenerative Diseases: Mitochondrial Dysfunction and Oxidation Damage (Neuroscience Intelligence Unit Series). Landes Bioscience, 1995.

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10

(Editor), Yau-Huei Wei, ed. The Role of the Mitochondria in Human Aging and Disease: From Genes to Cell Signaling (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2005.

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11

Oxidative Stress, Mitochondrial Dysfunction, and Novel Therapies, An Issue of Veterinary Clinics: Small Animal Practice. Saunders, 2008.

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12

Aliev, Gjumrakch. Role of Oxidative Stress, Mitochondria Failure, and Cellular Hypoperfusion in the Context of Alzheimer Disease: Past, Present and Future. Nova Science Publishers, Incorporated, 2013.

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13

Feeney, Chris. Astrocyte function in pathophysiological states: Free radical production and mitochondrial dysfunction during oxidative stress and oxygen-glucose deprivation. 2003.

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14

Zilliox, Lindsay, and James W. Russell. Diabetic and Prediabetic Neuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0115.

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Impaired glucose regulation (IGR) constitutes a spectrum of impaired glucose and metabolic regulation that can result in neuropathy. Several different pathways of injury in the diabetic peripheral nervous system that include metabolic dysregulation induced by metabolic syndrome induce oxidative stress, failure of nitric oxide regulation, and dysfunction of certain key signaling pathways. Oxidative stress can directly injure both dorsal route ganglion neurons and axons. Modulation of the nitric oxide system may have detrimental effects on endothelial function and neuronal survival. Reactive oxi

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15

Hinder, Lucy M., Kelli A. Sullivan, Stacey A. Sakowski, and Eva L. Feldman. Mechanisms Contributing to the Development and Progression of Diabetic Polyneuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0114.

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Advances in our understanding of diabetes in human patients and experimental models indicate that a number of mechanisms may contribute to sensory nerve damage in diabetic polyneuropathy (DPN). In addition to oxidative stress, hyperglycemia and hyperlipidemia, recent research in pain, advanced glycation endproduct (AGE), and proteomics specify a contributory role for altered neuronal calcium homeostasis in DPN. Technology advances indicate neuronal energy balance and mitochondrial biogenesis, fission, and fusion are additional potential mechanisms. The effects of dysregulation or loss of insul

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16

Gray, Doug, Carole Proctor, and Tom Kirkwood. Biological aspects of human ageing. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0001.

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At the molecular and cellular levels human ageing is characterized by the accumulation of unrepaired random damage, and an accompanying loss of function. A major source of damage is oxidative stress caused by the generation of reactive oxygen species as a by-product of respiration. DNA and proteins are both susceptible to damage but whereas DNA damage repair systems exist, faulty proteins are generally removed by protein degradation systems. During ageing these systems become less efficient and the subsequent accumulation of damaged protein promotes protein aggregation, a process which is espe

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17

Poff, Angela M., Shannon L. Kesl, and Dominic P. D’Agostino. Ketone Supplementation for Health and Disease. Edited by Dominic P. D’Agostino. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0032.

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Exogenous ketone supplements rapidly elevate blood ketones in a dose-dependent manner regardless of dietary intake, making them a practical method of inducing therapeutic ketosis for medical use. It is thought that ketone supplementation could be used as a stand-alone therapy, or as a way to further augment the therapeutic efficacy of the ketogenic diet. Ketone supplementation could increase treatment compliance by allowing many patients to maintain a more normal lifestyle with a less restrictive diet. The therapeutic effects of ketone supplementation are likely mediated in part by a stabiliza

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18

Berdanier, Carolyn D. Mitochondria in Health and Disease. Oxidative Stress and Disease Series. Taylor & Francis Group, 2010.

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19

Hausenloy, Derek, and Derek Yellon, eds. Novel Cardioprotective Strategies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0011.

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• Despite optimal therapy, the mortality and morbidity of coronary heart disease remains significant. Hence, novel treatment strategies of cardioprotection are required to improve clinical outcomes in these patients• Experimental studies have provided a plethora of therapeutic strategies for reducing myocardial injury, but the translation of these findings into the clinical setting has been largely disappointing. Many of these unsuccessful clinical studies have relied upon individually targeting established mediators of lethal reperfusion injury such as oxidative stress, inflammation, calcium

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20

Ebadi, M. Oxidative Stress in Mitochondria Disorders of Aging: Mitochondria Control Cell Death (Biological Signals and Receptors, 1-2). Not Avail, 2001.

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21

Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, a

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22

Ebadi, M. Oxidative Stress in Mitochondria Disorders of Aging: Mitochondria in Disease Stats (Biological Signals and Receptors 2001, Volume 10, Numbers 3-4). S Karger Pub, 2001.

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23

Jaiswal, Manoj Kumar, ed. The Role of Mitochondria, Oxidative Stress and Altered Calcium Homeostasis in Amyotrophic Lateral Sclerosis: From Current Developments in the Laboratory to Clinical Treatments. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-146-3.

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24

Human Longevity: Omega-3 Fatty Acids, Bioenergetics, Molecular Biology and Evolution. Taylor & Francis Group, 2014.

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25

Valentine, Raymond C., David L. Valentine, and R. C. Valentine. Human Longevity. Taylor & Francis Group, 2014.

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26

Valentine, Raymond C., and David L. Valentine. Human Longevity: Omega-3 Fatty Acids, Bioenergetics, Molecular Biology, and Evolution. Taylor & Francis Group, 2014.

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27

Valentine, Raymond C., and David L. Valentine. Human Longevity: Omega-3 Fatty Acids, Bioenergetics, Molecular Biology, and Evolution. Taylor & Francis Group, 2014.

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