Oxidative stress : diagnostics, prevention, and therapy vol 2

543 Pages·2015·9.886 MB·English

by  Hepel, Maria, Andreescu, Silvana

Oxidative Stress: Diagnostics,
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In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.
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In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.
1200
ACS SYMPOSIUM SERIES
Oxidative Stress: Diagnostics,
Prevention, and Therapy
Volume 2
1
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w Maria Hepel, Editor
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20 SUNY Potsdam
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15- Potsdam, New York
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1/ Silvana Andreescu, Editor
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AmericanChemicalSociety,Washington,DC
DistributedinprintbyOxfordUniversityPress
In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.
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Oxidativestress:diagnostics,prevention,andtherapy/SilvanaAndreescu,MariaHepel,
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00.f p.cm.
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1 Includesbibliographicalreferencesandindex.
15- ISBN978-0-8412-3100-9(acid-freepaper) 1. Oxidativestress--Physiologicaleffect.2.
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2 Antioxidants. I.
k-
b Andreescu,Silvana.II.Hepel,Maria.III.AmericanChemicalSociety.Divisionof
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In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.
Foreword
The ACS Symposium Series was first published in 1974 to provide a
mechanism for publishing symposia quickly in book form. The purpose of
the series is to publish timely, comprehensive books developed from the ACS
sponsoredsymposiabasedoncurrentscientificresearch. Occasionally,booksare
01 developed from symposia sponsored by other organizations when the topic is of
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In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.
Preface
Following the edition of the first volume of Oxidative Stress: Diagnostics,
Prevention, and Therapy, which was met with great interest, Volume 2 of this
series covers the latest achievements in diagnosis, prevention, and therapy
of oxidative stress and related diseases. The book provides a comprehensive
1 overview of the oxidative stress related mechanisms in biological systems and
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0
pr the involvement of reactive oxygen and nitrogen species (ROS and RNS), the
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0 damage of DNA, proteins, and lipids caused by oxidative stress, the protection
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1
5- of cells and tissues against free radicals, the relation of the oxidative stress to
1
20 aging and human diseases including cancer and neurological disorders, and the
bk- development of new therapeutic approaches to modulate oxidative stress. The
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2 current state-of-the-art methodologies including the development of sensors and
0
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0. biosensors for the detection of ROS/RNS and of biomarkers of oxidative stress
1
oi: are also discussed. The book is organized in three overlapping parts, starting
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5 | with general considerations of the oxidative stress, homeostasis pathways, and
01 ROS mechanisms, followed by chapters discussing the involvement of ROS in
2
3, particular diseases and concluding with analytical aspects of oxidative stress
1
er monitoring. The book provides a solid background on oxidative stress and
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cto ROS/RNS generation for novice learners while also offering scientists and
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b): practitioners already involved in this field a wealth of information covering the
e most recent developments in the study of oxidative stress, the role of radical
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e ( species, novelantioxidanttherapies, andmethodsforassessingfreeradicalsand
Dat oxidative stress. We sincerely hope that this book will find a wide audience
on of scientists searching for a useful collection of critical reviews related to the
cati expandingfieldofoxidativestress.
bli
Pu

Maria Hepel
SUNYPotsdam
Potsdam, NewYork
SilvanaAndreescu
ClarksonUniversity
Potsdam, NewYork
ix
In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.
Editors’ Biographies
Maria Hepel
Maria Hepel received her M.S. and Ph.D. in chemistry from Jagellonian
University in Krakow, Poland. Beginning in 1985, she worked as part of the
faculty at the State University of New York at Potsdam where she is now
01 a professor and Chair of the Department of Chemistry. She has published
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ot more than 160 papers and 44 chapters in books, and she has made more
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20 than 400 presentations at national and international symposia. Her current
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5- research interests are multidisciplinary and include DNA intercalation sensors,
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2 piezoimmunosensors, sensors for biomarkers of oxidative stress and cancer,
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b fluorescence energy transfer (FRET and NSET), DNA-hybridization biosensors,
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02 microsensor arrays, controlled drug release systems, nanotechnology, dye
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0. pollutant degradation, supercapacitors and electrochromic devices. She won
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oi: the SUNY Potsdam President’s Award for Excellence in Research and Creative
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5 | Endeavor in 1995 and 2001, the SUNY Chancellor’s Award for Excellence in
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0 Teachingin1998,andtheSUNYChancellor’sAwardforResearchin2003. She
2
3, wasalsoawardedthe2012NortheastRegionACSAwardforAchievementsinthe
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er ChemicalScience. In2013,shewasnamedaSUNYDistinguishedProfessorand
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ct became a member of the SUNY Distinguished Academy and SUNY Excellence
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b): Network.
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blic Silvana Andreescu is the Egon Matijević Endowed Chair in Chemistry in
Pu the Department of Chemistry and Biomolecular Science at Clarkson University.

Herresearchinterestsincludebiosensors,bioanalyticalapplicationsofmetaland
metal oxide nanoparticles, and the development of microelectrochemical probes
for studying physiological mechanisms in biological systems. Her recent work
involved study of the nanoceria chemistry, the mechanism of the antioxidant

activityoftheseparticles,andthedevelopmentofprobesformonitoringreactive
oxygenspeciesandoxidativestressinbiologicalmodelsystems.
©2015AmericanChemicalSociety
In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.
©2015AmericanChemicalSociety
ROS present in cells and blood during disease onset and progression, and even
pathogenicorigin(8,9). Newexperimentaltoolsareaidingnowindiscoveriesof
diseases, for instance, those developing in the brain (5–7) or those without any
byoxidativestress(1–4). Oxidativestresshasalsobeenimplicatedinmanyother
rangeofdiseases. Manyillnessescausedbyinflammationmayinfactbeinduced
involvement of oxidative stress and reactive oxygen species (ROS) in a wide
Extensive studies carried out in the field of pathogenesis indicate the
Introduction
discussed.
has been implicated, such as cancer and diabetes are also
01 multipleorgansandsystemicdiseasesinwhichoxidativestress
0
ch organs, joints, skin, and blood. Diseases that spread over
0.
0 nervous system, heart, lungs, kidneys, liver, reproductive
2
1
5- consequences in the development of diseases of the central
1
20 proteins and lipids as a result of oxidative stress and their
bk- antioxidant defense system. We discuss changes in DNA,
1/
2 the imbalance between the ROS/RNS production and the
0
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0. and Nitrogen Species (ROS/RNS), ROS/RNS toxicity and
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oi: consider processes involving the release of Reactive Oxygen
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5 | stress within cells, tissues, organs and whole organisms. We
01 an overview of the processes and consequences of oxidative
2
3, progression of many diseases. In this Chapter, we provide
1
er that oxidative stress plays a critical role in the initiation and
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Dat *E-mail: [email protected](M.H.),[email protected](S.A.)
on Potsdam,NewYork13699-5810
ublicati 2DepartmentofChemistPryotasnddamB,ioNmewoleYcourlakr1S3c6i7e6nce,ClarksonUniversity,
P
1DepartmentofChemistry,StateUniversityofNewYorkatPotsdam,
MariaHepel andSilvanaAndreescu
1,* 2,*
Oxidative Stress and Human Health
Chapter 1
In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.
2
bytheantioxidantpowerofROSscavengers,asillustratedinFig. 1.
Undersustainableredoxconditions,thegenerationofROSmustbebalanced
RedoxHomeostasis
side effects.
whichcurrentlythereisnocureorthepresenttreatmentsareobscuredwithserious
manydiseasesandtodevelopnewtherapiestohelpmanagingtheconditionsfor
atthecellularlevelisessentialtogainbetterunderstandingofthepathogenesisof
Unravelingthesignalingmechanismsinvolvingoxidativestressmessengers
processes.
islikelycausedbyinhibitionofproteinsynthesis,DNAreplication,andotherlife
generation of ROS or Fe(II) during the pathogen attack suggesting that lethality
1
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0 inducing ROS (26, 27), others (28, 29) have shown that there is no increased
h
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0. subject to controversy. While some believe that antibiotics kill bacteria by
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12 Whether antibiotics kill bacteria by an oxidative stress mechanism is also
5-
1 cellularantioxidantresponses(25).
0
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1/ ozonemayinducecancer. TheincreaseinROSstressorlevelsinelderly,suffering
2
10 (24). However,suchcasesarenotwithoutcontroversysinceevenalowdoseof
0.
1 an ozone therapy has been applied showing some improvement in redox status
doi: reducethechronicoxidativestressinelderlypatientswithcardiovasculardisease,
5 | anti-oxidative responses in a process called hormesis (22, 23). For instance, to
1
0
2 shock") may also be beneficial in deterrence of aging by inducing natural
3,
1 have been developed in cells. The short-term oxidative stress (or "oxidative
er
b mechanisms(20)andpathwaystoinitiateapoptosis(21),ifDNAisunrepairable,
o
Oct proteins (19). To avert the propagation of mutations, various DNA repair
b): in physiological processes may contribute to the damage of DNA, lipids, and
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W UV light or ionizing radiation (18), as well as the internal ROS generation
ate ( heavy metal ions, herbicides and pesticides, photosensitizers, etc.) (15–17),
D
n Prolonged exposure to environmental pollutants (strong oxidizing agents,
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ati dismutase,glutathioneperoxidase,catalaseandothers.
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P such as ultraviolet radiation, cigarette smoking, alcohol, or drugs. The enzymes

metabolicactivities. ROSareproducedinresponsetoenvironmentalconditions,
macrophages(14)duringinflammationandinotherprocessesofnormalcellular
reticulum (12). The generation of ROS takes also place in neutrophils (13) and
mitochondriaintheelectrontransferchainreactions(10,11)andinendoplasmic
are formed as intermediates and by-products in the energy production cycle in
insufficientanti-oxidantcapacityoftheredoxhomeostasissystem. ROSspecies
pathogenic defenses or generated at normal levels but not neutralized due to the
TheexcessamountsofROSareeitherproducedintheorganismoncallfor
developinginallorgansofthehumanbody.
the contribution of the oxidative stress to the pathogenesis of common diseases
themechanismofreleaseofROS/RNSspecies,meansoftheirneutralization,and
longbeforetheappearanceofdiseasesymptoms. Inthisreview,wehaveanalyzed
In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.
3
to optimize cellular defenses. The major components playing important roles in
antioxidants can also influence gene expression associated with stress responses
by modulating processes from mitosis to senescence and death. These cellular
organizationofdefense,enzymaticactivity,aswellasthegrowthanddevelopment
are redox buffers that interact with various cellular components influencing the
biomolecule antioxidants, such as glutathione, tocopherol, and ascorbic acid,
modifications are critically important for the control of protein functions. Small
state of the biological environment can readily modify those proteins and these
groupsordislphidebondscanactastheredoxsensorsandeffectorssinceredox
in different tissues, cells, and organelles. Many proteins that contain sulfhydryl
ofautonomousreplenishmentofantioxidantsstoredandsynthesized(expressed)
redox-potential homeostasis is a complex one and it consists of many pathways
is generally a balanced process. The actual mechanism of operation of the
systems are found in all living organisms, one can say that the ROS generation
1
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0 system must be established in any healthy organism. Since such homeostasis
h
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0. immunedeficiencystate. Thismeansthatanactiveredox-potentialhomeostasis
0
12 of the antioxidant counterbalance to prevent slipping into an oxidative stress or
5-
1 AnychangeinROSproductionmustbemetwiththerespectiveadjustment
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In Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2; Hepel, et al.;
ACS Symposium Series; American Chemical Society: Washington, DC, 2015.