editorial harmful and beneficial role of rosdownloads.hindawi.com/journals/omcl/2016/7909186.pdf ·...

EditorialHarmful and Beneficial Role of ROS

Sergio Di Meo,1 Tanea T. Reed,2 Paola Venditti,1 and Victor M. Victor3

1Dipartimento di Biologia, Universita di Napoli “Federico II”, 80126 Napoli, Italy2Department of Chemistry, Eastern Kentucky University, Richmond, KY 40475, USA3Service of Endocrinology, Dr. Peset University Hospital, Foundation for the Promotion of Health and Biomedical Research inthe Valencian Region (FISABIO), 46010 Valencia, Spain

Correspondence should be addressed to Sergio Di Meo; [email protected]

Received 20 June 2016; Accepted 20 June 2016

Copyright © 2016 Sergio Di Meo et al. This is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reactive oxygen species (ROS) are an unavoidable byproductof oxygen metabolism and their cellular concentrations aredetermined by the balance between their rates of productionand their rates of clearance by various antioxidant com-pounds and enzymes. For a long time ROS were thoughtto cause exclusively toxic effects which were associated withvarious pathologies, including carcinogenesis, neurodegen-eration, atherosclerosis, diabetes, and aging. However, todate, it is known that while prolonged exposure to highROS concentrations may lead to various disorders, lowROS concentrations exert beneficial effects regulating cellsignaling cascades.

The papers reported in this issue focus attention on someaspects of ROS biology including the impact of ROS produc-tion on various body districts and the defense arising fromendogenous and exogenous antioxidants, beneficial effects ofROS production, and ROS regulation of signaling pathways.However, the examination of the manuscripts clearly showsthat the passage of time has partly changed the approach tovarious topics. For example, although in someworks differentsubstances, including antioxidants, have yet been used, inother works different procedures and substances, includingproducts or extracts, have been successfully used in thetreatment of oxidative stress and related disorders due to thecomplex bioactive compounds they contain.

Thus,A.V.Maksimenko studied the effects of intravenousinjection of the superoxide dismutase-chondroitin sulfate-catalase (SOD-CHS-CAT) conjugate in a rat model of endo-toxin shock. In this way he demonstrated the effectivenessof the conjugate in prevention and medication of oxidativestress damage, which is only partly due to prevention of NOconversion in peroxynitrite.

The review of V. D. Prokopieva et al. examined proper-ties and biological effects of the antioxidant carnosine andpresented data on successful use of carnosine in differentpathologies. Such data show that carnosine is an effectiveantioxidant able to protect tissues against various adversefactors inducing development of oxidative stress.

S. Ponist et al. evaluated the therapeutic potential ofcarnosine in rat adjuvant arthritis. The results obtained ontwo animal models (model of local acute inflammatory reac-tion and subchronic model of rodent polyarthritis) showedthat carnosine had systemic anti-inflammatory activity andprotected rat brain and chondrocytes from oxidative stress.

A.Matuszyk et al. found that administration of exogenousobestatin accelerates the healing of acetic acid-induced col-itis, an effect partly due to anti-inflammatory properties ofobestatin that reduces IL-1𝛽 concentration and myeloperoxi-dase activity in colonic mucosa.

C. Liu et al. used the aqueous extract of Cordyceps mil-itaris fruit body in streptozotocin-induced diabetic rats andfound that the extract displays antidiabetic and antinephroticactivity due to its ability to attenuate oxidative stress.

W. J. Bae et al. examined the effects of decursin extractedfrom Angelica gigas Nakai (AG) on antioxidant activityin vitro and in a cryptorchidism-induced infertility ratmodel. Their study suggests that decursin is able to reduceoxidative stress by Nrf2-mediated upregulation of hemeoxygenase-1 (HO-1) in rat experimentally induced unilateralcryptorchidism and may improve cryptorchidism-inducedinfertility.

E. Kerasioti et al. studied the protective effect ofsheep whey protein (SWP) against tert-butyl hydroperoxide-(tBHP-) induced oxidative stress in endothelial cells. Their

Hindawi Publishing CorporationOxidative Medicine and Cellular LongevityVolume 2016, Article ID 7909186, 3 pageshttp://dx.doi.org/10.1155/2016/7909186

2 Oxidative Medicine and Cellular Longevity

findings demonstrate that SWP protects endothelial cellsfrom oxidative stress increasing GSH levels and decreasingGSSG, lipid peroxidation, protein oxidation, and ROS levels.

P. Boonruamkaew et al. studied the effect of an antiox-idative nanoparticle (RNPN) that they recently developedagainst APAP-induced hepatotoxicity in mice. Their findingslead to concluding that RNPN possesses effective hepatopro-tective properties and does not exhibit the notable adverseeffects associated with NAC treatment.

M. J. Gomes et al. evaluated the influence of exerciseon functional capacity, cardiac remodeling, and skeletalmuscle oxidative stress in rats with aortic stenosis- (AS-)induced heart failure (HF).They found that exercise improvesfunctional capacity in rats regardless of echocardiographicparameter changes. In soleus, exercise reduces oxidativestress, preserves antioxidant enzyme activity, and modulatesmitogen-activated protein kinases (MAPK) expression

S. Kremserova et al. evaluated the role ofmyeloperoxidase(MPO) in the regulation of acute lung inflammation andinjury. They showed that MPO deficiency enhances neu-trophilia during LPS-induced airway inflammation due toaltered accumulation of proinflammatory cytokine RANTES(regulated on activation, normal T cell expressed andsecreted) and reduces cell death of MPO deficient neu-trophils. The role of MPO in the regulation of the course ofpulmonary inflammation, independent of its putative micro-bicidal functions, can be potentially linked to its ability tomodulate the life span of neutrophils and affect accumulationof chemotactic factors at the site of inflammation.

J. Petrovic et al. investigated whether magnesium supple-mentation in sedentary and rugby players young men couldprotect peripheral blood lymphocytes (PBL) from hydrogenperoxide-inducedDNAdamage.They found thatmagnesiumsupplementation has marked effects in protecting the DNAfrom oxidative damage in both men with different lifestyles.

T. Kataoka et al. compared the mitigating effects onchronic constriction injury- (CCI-) induced neuropathicpain of radon inhalation and pregabalin administration andexamined the combination effects of the treatments. Theyfound that combined effect of radon and pregabalin is anadditive effect because it has mitigative effect similar to theeffects of remarkably higher dose of pregabalin. The possi-ble mechanism is the activation of antioxidative functionsinduced by radon inhalation.

G. Espinha et al. found that the inhibition of RhoAGTPase, an enzyme overexpressed in highly aggressivemetastatic tumors, increases sensitivity of melanoma cells toUV radiation effects, suggesting that this GTPase representsa potential inhibitory target for metastatic melanomas.

Some works have addressed the problem of the dual roleplayed by ROS or ROS producing enzymes.

N. Kaludercic and V. Giorgio described mitochondriaas a major site of production and as a target of ROS/RNSand discussed how the posttranslational modifications ofATP synthase due to ROS/RNS generation might play a dualrole by promoting cell death or survival depending on theirrelative effects on mitochondrial ATP synthase catalysis andPTP.

H. Pei et al. summarized the present understanding ofthe role played by mitochondrial functional proteins such

as electron transport chain complexes, uncoupling proteins,mitochondrial dynamic proteins, translocases of outer mem-brane complex, and mitochondrial permeability transitionpore in ROS production and in protection of mitochondrialintegrity and function in ischemic heart diseases.

M. G. Battelli et al. reviewed the physiological andpathological roles of xanthine oxidoreductase- (XOR-)derived oxidant molecules showing that they may resultin either harmful or beneficial outcomes. Indeed, XORgenerates free radicals which are responsible for tissuedamage in hypoxia/reoxygenation and ischemia/reperfusion,have proinflammatory activity, are involved in cancerpathogenesis, and favor the progression to malignancy byinducing angiogenesis and cell migration. On the otherhand, XOR products may activate the expression of theproapoptotic protein p53 and transcription factors withantitumorigenic and antiproliferative activity.

H.-Y. Tan et al. reviewed the role of ROS in maintainingthe homeostatic functions of macrophage and in particularmacrophage polarization. They also reviewed the biology ofmacrophage polarization and the disturbance of the balanceof the different functional phenotypes in human diseases.

J. A. Hernandez et al. reviewed the role of lipids in theneuronal damage induced by ethanol-related oxidative stressand in the related compensatory or defense mechanisms.They showed that ethanol-induced neurodegeneration is atleast partly the result of the equilibrium between the toxicityof signaling lipids and the protection that some lipids, suchphosphatidylethanolamine and cholesterol, confer to the cell.

A. Schmidt et al. used a HaCaT keratinocyte cell culturemodel to investigate redox regulation and inflammation toperiodic, low-dose oxidative challenge generated by recurrentincubation with cold physical plasma-treated cell culturemedium. They investigated the HaCaT keratinocyte globaltranscriptomic profile over three months to identify genesresponsible for adaptations to periodic oxidative stress as seenin redox-related diseases of the skin.Their results suggest thatall keratinocytes may have adapted to redox stress over time,significantly altering their basal gene expression profile.

E. Ershova et al. studied the influence of a water-solublefullerene derivative (F828) on serum-starving human embryolung diploid fibroblasts HELFs.They found that F828 exerts ablock on genotoxic effect of oxidative stress in serum-starvingHELFs. The decrease in the number of double strand breaksand apoptosis was maximum at concentrations 0.2–0.25𝜇M,whereas, at concentrations higher than 0.5𝜇M, excessive ROSscavenging was accompanied by increased cell death rate.

The problem of the role of reactive species sources inhealth anddiseasewas examined by S.DiMeo et al.They, afterexamining the cellular localization and supposed involve-ment of such sources in tissue dysfunction and protection,examined experimental evidence concerning their harmfuland protective effects in a normal physiological activity, suchas exercise, and in pathologic conditions, such as diabetes andneurodegenerative diseases.

Some works have faced different problems that are stillunited by the oxidative stress impact on various pathologicalconditions and the factors involved in the signaling pathways

N. T. Costa et al. evaluated the involvement of TNF-𝛼 andinsulin resistance (IR) in the inflammatory process, oxidative

Oxidative Medicine and Cellular Longevity 3

stress, and disease activity in patients with rheumatoidarthritis (RA). They demonstrated that IR and TNF-𝛼 areimportant factors involved in redox imbalance in patientswith RA which seems to be due to the maintenance ofinflammatory state and disease activity.

S. Vrankova et al. studied the effects of NF-kB inhibitionon ROS and NO generation and blood pressure (BP) reg-ulation in hereditary hypertriglyceridemic rats. They foundthat NF-kB inhibition leads to decreased ROS degradation bySOD followed by increased heart oxidative damage and BPelevation despite the increase in eNOS protein.

L. Minutoli et al. described the current knowledge on therole of NLRP3 inflammasome in some organs (brain, heart,kidney, and testis) after I/R injury, with particular regard tothe role played by ROS in its activation. They conclude that adefinite comprehension of the role of NLRP3 inflammasomein the host responses to different danger signals is still lacking.

S. Kazemi et al. investigated the effects of the xenoe-strogenic chemical Bisphenol A (BPA) on hepatic oxidativestress-related gene expression in rats. Their finding demon-strated that BPA generates ROS and increases the expressionof HO-1 and Gadd45b genes that cause hepatotoxicity.

A. N. Onyango reviewed the potential pathways of theendogenous formation of singlet oxygen and ozone, theirrelevance to human health, and how dietary factors affectgeneration and activity of such oxidants.

E. Gammella et al. described the multifaceted systemsregulating cellular and body iron homeostasis and discussedhow altered iron balance may lead to oxidative damage insome pathophysiological settings.

X.Wang et al. found that the transcription factor BTB andCNC homology 1 (Bach1) induces endothelial cell apoptosisand cell cycle arrest through ROS generation and, conse-quently, that functional downregulation of Bach1 may be apromising target for the treatment of vascular diseases.

M. Nita and A. Grzybowski, examining the currentliterature, showed that excessive production of reactive oxy-gen species and oxidative stress play important role in thepathogenesis of many age-related ocular diseases and otherpathologies of the anterior and posterior eye segment inadults. ROS stimulate cells’ death via apoptosis process,participate in the activation of proinflammatory and proan-giogenic pathways, and are associated with the autophagyprocess.

T. R. S. Hamilton et al. evaluated lasting effects of heatstress-induced oxidative stress on ejaculated and epididymalspermand found that it leads to rescuable alterations after onespermatic cycle in ejaculated sperm and also after 30 days inepididymal sperm.

M. L. Fanjul-Moles and G. O. Lopez-Riquelme exam-ined the relationships between oxidative stress, circadianrhythms, and retinal damage in humans, particularly thoserelated to light and photodamage. Their review highlightsthe role of oxidative stress as one of the main causes of age-related macular degeneration (AMD) etiologies, a disease towhich, in addition to genetic predispositions, at least fourprocesses contribute: lipofuscinogenesis, drusogenesis, localinflammation and neovascularization, and immunologicalmechanisms.

H. Nagahisa et al. studied structural and functionalchanges induced by SOD1 deficiency and their results sug-gested that muscle is damaged by ROS produced in theTypeIIx/b fibers of the gastrocnemius muscle, acceleratingthe proliferation and differentiation of satellite cells in SOD1KO mice.

It is our opinion that the articles included in this specialissue, despite dealing with so different topics, represent animportant contribution to the knowledge of the harmful andbeneficial effects of ROS in living organisms.

Sergio Di MeoTanea T. ReedPaola Venditti

Victor M. Victor

Submit your manuscripts athttp://www.hindawi.com

Stem CellsInternational

Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014


MEDIATORSINFLAMMATION

of


Behavioural Neurology

EndocrinologyInternational Journal of



Disease Markers


BioMed Research International

OncologyJournal of



Oxidative Medicine and Cellular Longevity


PPAR Research

The Scientific World JournalHindawi Publishing Corporation http://www.hindawi.com Volume 2014

Immunology ResearchHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014

Journal of

ObesityJournal of



Computational and Mathematical Methods in Medicine

OphthalmologyJournal of


Diabetes ResearchJournal of



Research and TreatmentAIDS


Gastroenterology Research and Practice


Parkinson’s Disease

Evidence-Based Complementary and Alternative Medicine

Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com

editorial harmful and beneficial role of rosdownloads.hindawi.com/journals/omcl/2016/7909186.pdf ·...

Documents