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1

service), ScienceDirect (Online, ed. Mitochondrial function: Mitochondrial electron transport complexes and reactive oxygen species. Amsterdam: Academic Press/Elsevier, 2009.

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2

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

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3

Schmitt, Franz-Josef, and Suleyman I. Allakhverdiev, eds. Reactive Oxygen Species. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781119184973.

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4

Espada, Jesús, ed. Reactive Oxygen Species. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0896-8.

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5

Schmidt, Harald H. H. W., Pietro Ghezzi, and Antonio Cuadrado, eds. Reactive Oxygen Species. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68510-2.

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6

Singh, Vijay Pratap, Samiksha Singh, Durgesh Kumar Tripathi, Sheo Mohan Prasad, and Devendra Kumar Chauhan, eds. Reactive Oxygen Species in Plants. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119324928.

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7

Rio, Luis Alfonso, and Alain Puppo, eds. Reactive Oxygen Species in Plant Signaling. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00390-5.

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8

Bhattacharjee, Soumen. Reactive Oxygen Species in Plant Biology. New Delhi: Springer India, 2019. http://dx.doi.org/10.1007/978-81-322-3941-3.

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9

Gilbert, Daniel L., and Carol A. Colton. Reactive Oxygen Species in Biological Systems. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/b113066.

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10

Smirnoff, Nicholas, ed. Antioxidants and Reactive Oxygen Species in Plants. Oxford, UK: Blackwell Publishing Ltd, 2005. http://dx.doi.org/10.1002/9780470988565.

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11

Catala, Angel. Reactive oxygen species, lipid peroxidation, and protein oxidation. New York: Nova Publishers, 2014.

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12

Gupta, S. Dutta. Reactive oxygen species and antioxidants in higher plants. Enfield, NH: Science Publishers, 2010.

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13

Quintanilha, Alexandre, ed. Reactive Oxygen Species in Chemistry, Biology, and Medicine. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-0417-4.

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14

Singh, Ranji. Reactive oxygen species and aluminum stress in Pseudomonas Fluorescens. Sudbury, Ont: Laurentian University, 2003.

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15

Gupta, Kapuganti Jagadis, and Abir U. Igamberdiev, eds. Reactive Oxygen and Nitrogen Species Signaling and Communication in Plants. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-10079-1.

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16

Gupta, Dharmendra K., José M. Palma, and Francisco J. Corpas, eds. Reactive Oxygen Species and Oxidative Damage in Plants Under Stress. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20421-5.

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17

Forman, Henry Jay, Jon Fukuto, and Martine Torres, eds. Signal Transduction by Reactive Oxygen and Nitrogen Species: Pathways and Chemical Principles. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/0-306-48412-9.

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18

Cromie, Lillian. The influence of reactive oxygen species on human lymphoid cell function in vitro. [s.l: The Author], 1991.

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19

Chapman, Sandy. Mechanisms of endothelin-1 induced reactive oxygen species production in vascular adventitial fibroblasts. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2008.

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20

McQuaid, Karen E. Acute modulation of endothelial cell barrier function by reactive oxygen and nitrogen species. Dublin: University College Dublin, 1997.

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21

Khan, M. Iqbal R., and Nafees A. Khan, eds. Reactive Oxygen Species and Antioxidant Systems in Plants: Role and Regulation under Abiotic Stress. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5254-5.

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22

Blount, Susan. Damage to DNA by reactive oxygen species: Relevance to the pathogenesis of systemic lupus erythematosus. Birmingham: University of Birmingham, 1991.

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23

Lo, Yvonne Yim Chung. Reactive oxygen species as signaling molecules regulating chondrocyte gene expression of fox, jun and collagenase. Ottawa: National Library of Canada, 1995.

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24

Musonda, Alam Clement. Quercetin as a modulator of xenobiotic metabolism and reactive oxygen species (ROS) in human hepG2 cells. Birmingham: University of Birmingham, 1998.

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25

Goldstone, Jared Verrill. Direct and indirect photoreactions of chromophoric dissolved organic matter: Roles of reactive oxygen species and iron. Cambridge, Mass: Massachusetts Institute of Technology, 2002.

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26

Wong, C. B. Henry. Involvement of reactive oxygen species and cytokines in nitric oxide production and apoptosis in bovine chondrocytes. Ottawa: National Library of Canada, 1999.

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27

Armstrong, D. Advanced protocols in oxidative stress III. New York: Humana Press, 2015.

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28

W, Allen Henry, and Culbert Michael L. 1937-, eds. Oxidology: The study of reactive oxygen toxic species (ROTS) and their metabolism in health and disease : the ROTS theory of degenerative disease and the HLB blood test. Los Altos, Calif: R.W. Bradford Foundation, 1985.

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29

Rea, Carol Anne. Glycation and the production of reactive oxygen species: Possible link in the pathogenesis of the vascular complications of diabetes. Birmingham: University of Birmingham, 1991.

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30

Advanced protocols in oxidative stress II. New York, N.Y: Humana Press, 2009.

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31

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

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32

Reactive Oxygen Species [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.94870.

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33

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 especially problematic in the ageing brain. Other aspects of ageing include genetic and epigenetic changes, mitochondrial dysfunction, telomere shortening, and cellular senescence, all subject to stochasticity. The complexity of the biology of ageing has led to an increase in the use of systems biology approaches whereby the use of mathematical modelling and bioinformatic tools complement the more traditional experimental approaches.
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34

McBurney, John W. Pesticides and Neurodegenerative Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.003.0008.

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Neurodegenerative diseases, which are characterized by neuronal degeneration, include Alzheimer disease (AD), Parkinson disease (PD), and amyotrophic lateral sclerosis (ALS). Their worldwide prevalence is increasing as the global population ages. The causes reflect interactions between genetics and environmental factors such as increasing urbanization, industrialization, and widespread use of chemicals, including insecticides, fungicides, and herbicides. Epidemiologic data suggest that exposure to many of these pesticides increases the risk of neurodegeneration. The best-defined mechanism for this association is mitochondrial toxicity resulting in increased reactive oxygen species. In PD and AD, the associated accumulation of aggregates of insoluble, misfolded proteins results in the formation of Lewy bodies and neurofibrillary tangles, respectively. Pesticide exposures can be reduced by modifying food choices and applying integrated pest management in schools, businesses, and homes. Medical professionals can counsel patients about limiting exposure to pesticides and decreasing the risk of neurodegenerative disorders.
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35

Reactive Oxygen Species In Plant Signaling. Springer, 2009.

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36

Bhattacharjee, Soumen. Reactive Oxygen Species in Plant Biology. Springer, 2019.

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37

1942-, Sies H., and Packer Lester, eds. Protein sensors and reactive oxygen species. San Diego, Calif: Academic Press, 2002.

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38

Reactive Oxygen Species and Male Fertility. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03936-025-3.

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39

Litell, John M., and Nathan I. Shapiro. Pathophysiology of septic shock. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0297.

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The pathophysiology of sepsis is the result of a dysregulated host response to infection. Interactions between conserved pathogenic signals and host recognition systems initiate a systemic reaction to local infection. Pro- and anti-inflammatory intermediates and associated coagulatory abnormalities lead to altered macrovascular, microvascular, and mitochondrial function. Uncorrected, these processes yield similar patterns of failure in multiple organ systems. Mortality increases with successive organ failures. Although commonly thought to be a manifestation of impaired renal circulation, septic acute kidney injury may be due primarily to non-haemodynamic factors. Pulmonary parenchymal dysfunction in sepsis also contributes to failures in other organ systems. Sepsis involves complex alterations in myocardial function, vascular tone, and capillary integrity, which are mediated by elevated concentrations of inflammatory cytokines, inducible nitric oxide, and reactive oxygen species, among others. Gut hypomotility and translocation of enteric flora likely contribute to a persistent inflammatory response. This perpetuates the pathophysiological pattern of sepsis, and can lead to the delayed onset of these features in patients with other types of critical illness. The neurological manifestations of sepsis include acquired delirium, which is also probably due to circulatory and inflammatory abnormalities, as well as alterations in cerebral amino acid metabolism. Critical illness-related corticosteroid insufficiency and derangements in glucose metabolism are among the endocrine abnormalities commonly seen in septic patients. Restoration of homeostasis requires early haemodynamic resuscitation and aggressive infectious source control.
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40

Smirnoff, Nicholas. Antioxidants and Reactive Oxygen Species in Plants. Wiley & Sons, Incorporated, John, 2008.

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41

Smirnoff, Nicholas. Antioxidants and Reactive Oxygen Species in Plants. Wiley & Sons, Incorporated, John, 2008.

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42

N, Smirnoff, ed. Antioxidants and reactive oxygen species in plants. Oxford, UK: Blackwell Pub., 2005.

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43

Filip, Cristiana, and Elena Albu, eds. Reactive Oxygen Species (ROS) in Living Cells. InTech, 2018. http://dx.doi.org/10.5772/intechopen.69697.

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44

T, Quintanilha Alexandre, and NATO Advanced Study Institute on Oxygen Radicals in Biological Systems: Recent Progress and New Study Methods (1985 : Braga, Portugal), eds. Reactive oxygen species in chemistry, biology, and medicine. New York: Plenum Press, 1988.

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45

Gupta, S. Dutta. Reactive Oxygen Species and Antioxidants in Higher Plants. Taylor & Francis Group, 2010.

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46

Quintanilha, A. Reactive Oxygen Species in Chemistry, Biology, and Medicine. Springer, 2013.

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47

Hasanuzzaman, Mirza, Vasileios Fotopoulos, Kamrun Nahar, and Masayuki Fujita, eds. Reactive Oxygen, Nitrogen and Sulfur Species in Plants. Wiley, 2019. http://dx.doi.org/10.1002/9781119468677.

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48

Ahmad, Shamim I. Reactive Oxygen Species in Biology and Human Health. Taylor & Francis Group, 2016.

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49

Gupta, S. Dutta. Reactive Oxygen Species and Antioxidants in Higher Plants. Taylor & Francis Group, 2010.

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50

Experimental protocols for reactive oxygen and nitrogen species. Oxford: Oxford University Press, 2000.

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