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Books on the topic 'Systemic oxidative stress'

Author: Grafiati

Published: 18 April 2022

Last updated: 30 July 2025

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1

Ceballos-Picot, Iréne. Oxidative stress in neuronal death. Landes Bioscience, 1997.

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2

M, Matata Bashir, and Elahi Maqsood M, eds. Oxidative stress: A focus on cardiovascular disease pathogensis. Nova Science, 2010.

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3

Jay, Forman Henry, and Cadenas Enrique, eds. Oxidative stress and signal transduction. Chapman & Hall, 1997.

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4

F, Keaney John, ed. Oxidative stress and vascular disease. Kluwer Academic Publishers, 1999.

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5

Matata, Bashir M., and Maqsood M. Elahi. Oxidative stress: A focus on cardiovascular disease pathogensis. Nova Biomedical, 2011.

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6

Veasey, Sigrid C. Oxidative Neural Injury. Humana Press, 2009.

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7

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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8

Offen, Daniel. The molecular basis for neurodegenerative diseases. Research Signpost, 2007.

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9

NATO, Advanced Research Workshop on Frontiers in Neurodegenerative Disorders and Aging: Fundmental Aspects Clinical Perspectives and New Insights (2003 Antalya Turkey). Frontiers in neurodegenerative disorders and aging: Fundamental aspects, clinical perspectives and new insights. IOS Press, 2004.

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10

1945-, Favier Alain, ed. Analysis of free radicals in biological systems: Edited by A. E. Favier ... [et al.]. Birkhäuser Verlag, 1995.

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11

Crichton, Robert R. Metal-based neurodegeneration: From molecular mechanisms to therapeutic strategies. 2nd ed. John Wiley & Sons, 2013.

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12

M, LeVine Steven, Connor James R, and Schipper Hyman M. 1954-, eds. Redox-active metals in neurological disorders. New York Academy of Sciences, 2004.

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13

G, Poli, Packer Lester, and Cadenas Enrique, eds. Free radicals in brain pathophysiology. Dekker, 2000.

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14

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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15

Falk, Katherine, Barbara Bartlik, and Janet Mindes. Inflammation and the Gut–Brain–Mood Connection (DRAFT). Edited by Madeleine M. Castellanos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190225889.003.0014.

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Inflammation, oxidative stress, dysbiosis, and increased gut permeability (leaky gut) are now understood to be among the causative factors in depression, other psychiatric illnesses, and sexual dysfunction. This new appreciation of psychiatric illness as a systemic illness, occurring in the body as well as in the brain, offers new ways to understand and treat sexual problems such as polycystic ovary syndrome and erectile dysfunction. Leaky gut can be caused by medications such as antibiotics, NSAIDS, or aspirin; drinking alcohol; or the proinflammatory standard American diet. As conventional t

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16

Riederer, Peter, and S. H. Parvez. Oxidative Stress and Neuroprotection. Springer, 2014.

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17

Riederer, Peter, and S. H. Parvez. Oxidative Stress and Neuroprotection. Springer London, Limited, 2006.

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18

Pokorski, Mieczyslaw. Oxidative Stress and Cardiorespiratory Function. Springer International Publishing AG, 2016.

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19

Pokorski, Mieczyslaw. Oxidative Stress and Cardiorespiratory Function. Springer, 2014.

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20

Pokorski, Mieczyslaw. Oxidative Stress and Cardiorespiratory Function. Springer, 2014.

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21

Oxidative stress and neurodegenerative disorders. Elsevier, 2007.

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22

(Editor), G. Ali Qureshi, and S. Hasan Parvez (Editor), eds. Oxidative Stress and Neurodegenerative Disorders. Elsevier Science, 2007.

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23

Qureshi, G. Ali, and S. Hasan Parvez. Oxidative Stress and Neurodegenerative Disorders. Elsevier Science & Technology Books, 2007.

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24

Annane, Djillali, and B. Jérôme Aboab. Management of carbon monoxide poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0328.

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CO poisoning is the commonest cause of toxic death. Carbon monoxide is colourless, odourless, and tasteless, and is produced under various conditions. When people inhale CO, the gas diffuses rapidly to the body and replaces oxygen at the level of haemoglobin, myoglobin, and other oxygen carriers. Subsequently, CO causes oxygen deprivation of all body tissues. CO also induces oxidative stress and systemic inflammation. After CO poisoning a broad variety of symptoms may occur. Survivors of CO poisoning often present with persistent neurological sequels or develop delayed neurological symptoms. T

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25

Anti-Inflammatory Cookbook for Beginners: 250 Authentic, Easy, Healthy, and Tasty Recipes for Newbies and a 28-Day Meal Plan That Chooses Anti-inflammatory Foods in the Right Amounts to Reduce Oxidative Stress and the Risk of Systemic Inflammation. Independently Published, 2022.

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26

Yoshikawa, Toshikazu. Oxidative Stress and Digestive Diseases. S. Karger Publishers (USA), 2001.

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27

Gracia-Sancho, Jordi, and M. Josepa Salvadó. Gastrointestinal Tissue: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology Books, 2017.

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28

Gracia-Sancho, Jordi, and M. Josepa Salvadó. Gastrointestinal Tissue: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology Books, 2017.

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29

Ceballos-Picot, Irene. Role of Oxidative Stress in Neuronal Death. Springer London, Limited, 2013.

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30

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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31

Veasey, Sigrid C. Oxidative Neural Injury. Humana Press, 2010.

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32

Croft, Cassidy. Oxidative Stress: Causes, Role in Diseases and Biological Effects. Nova Science Publishers, Incorporated, 2016.

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33

Croft, Cassidy. Oxidative Stress: Causes, Role in Diseases and Biological Effects. Nova Science Publishers, Incorporated, 2014.

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34

The Role of Oxidative Stress in Neuronal Death. Landes Bioscience, 1997.

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35

Ceballos-Picot, Irene. The Role of Oxidative Stress in Neuronal Death. Springer, 2013.

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36

Oxidative Stress and Free Radical Damage in Neurology. Humana, 2012.

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37

(Editor), H. Parvez, and P. Riederer (Editor), eds. Oxidative Stress and Neuroprotection (Journal of Neural Transmission. Supplementa). Springer, 2006.

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38

Montagnier, Luc, Catherine Pasquier, and Rene Olivier. Oxidative Stress in Cancer, AIDS, and Neurodegenerative Diseases. Taylor & Francis Group, 1997.

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39

Montagnier, Luc, C. Pasquier, and René Olivier. Oxidative Stress in Cancer AIDS and Neurodegenerative Diseases. Taylor & Francis Group, 2019.

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40

Montagnier, Luc, Catherine Pasquier, and Rene Olivier. Oxidative Stress in Cancer, AIDS, and Neurodegenerative Diseases. Taylor & Francis Group, 1997.

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41

Packer, Lester, Enrique Cadenas, and Montagnier. Oxidative Stress in Cancer, AIDS, and Neurodegenerative Diseases. Taylor & Francis Group, 2019.

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42

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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43

Becker, Jeffrey. Nutraceutical Treatments for Addiction Recovery. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0020.

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Current medical treatment in substance-use disorders and addiction recovery often fails to address the underlying molecular pathophysiologic mechanisms of addiction morbidity. Psychopharmacology and behavioral interventions do not directly address the cellular patterns of dysfunction in addiction but natural treatments can and should be employed in a research-based manner to support existing treatment protocols. Research into addiction pathophysiology is clear: removing the offending agent through sobriety is often not enough to restore natural premorbid physiology. Drug-induced oxidative stre

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44

Jr, John F. Keaney. Oxidative Stress and Vascular Disease (Developments in Cardiovascular Medicine). Springer, 2000.

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45

Farooqui, Akhlaq A. A. Inflammation and Oxidative Stress in Neurological Disorders: Effect of Lifestyle, Genes, and Age. Springer, 2016.

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46

Farooqui, Akhlaq A. Inflammation and Oxidative Stress in Neurological Disorders: Effect of Lifestyle, Genes, and Age. Springer London, Limited, 2014.

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47

Farooqui, Akhlaq A. Inflammation and Oxidative Stress in Neurological Disorders: Effect of Lifestyle, Genes, and Age. Springer, 2014.

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48

Connor, James R. Metals and Oxidative Damage in Neurological Disorders. Springer London, Limited, 2013.

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49

(Editor), Lawrence Spatz, and Arthur D. Bloom (Editor), eds. Biological Consequences of Oxidative Stress: Implications for Cardiovascular Disease and Carcinogenesis (The Conte Institute Series, 1). Oxford University Press, USA, 1992.

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50

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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