Reactive Oxygen Species In Tissues Research Articles

The evaluation of oxidative stress and inflammation markers in serum and saliva of the patients with temporomandibular disorders.

Temporomandibular Disorders (TMD), as in the occurrence of many diseases, have been associated with oxidative stress (OS) resulting from the disruption of antioxidant mechanisms and the accumulation of reactive oxygen species in tissues. This study was designed to compare salivary and serum OS and inflammation markers of individuals with TMD and healthy subjects. A prospective cross-sectional study was conducted. Twenty-seven TMD patients diagnosed with disc displacement (DD) according to Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) and 17 healthy subjects were enrolled in the study. Prior to any treatment, serum, and saliva samples were taken from the patients and centrifuged, and stored at -80 °C until analyzed. All samples were examined for Interleukin-6 (IL-6), Malondialdehyde (MDA), and 8-hydroxydeoxyguanosine (8-OHdG) concentrations. There was no significant difference between the groups regarding median values of 8-OHdG, IL-6, and MDA (p > 0.05). When the relationship between serum and salivary 8-OHdG, IL-6, and MDA levels in all subjects was evaluated, there was a strong positive correlation between the levels of 8-OHdG and IL-6 in the serum (r = 0.752, p <0.001). In the study group, when the relationship between pain levels and serum and saliva 8-OHdG, IL-6, and MDA levels was assessed, a positive and strong correlation was found between the levels of 8-OHdG and IL-6 in serum. Although the strong correlation between pain scores and serum 8-OHdG and MDA levels supports the hypothesis that inflammation and OS mechanisms may be interrelated, according to the results of the study, inflammatory and OS markers in patients with TMD were not different from healthy individuals.

Adaptive photosynthetic strategies of the invasive plant Sphagneticola trilobata and its hybrid to a low-light environment

In stressful environments, invasive plants acclimate more efficiently than native plants and hybridization mainly contributes to this process. We examined changes in the morphological characteristics, photosynthetic characteristics, and antioxidant capacity of Sphagneticola trilobata and its hybrids in a low-light environment to explore their invasiveness, with Sphagneticola calendulacea serving as the control. The morphological plasticity of S. trilobata was not dominant, the maximal photochemical efficiency of PSII, actual quantum yield of PSII, and electron transport rate of PSⅡ increased and nonphotochemical quenching decreased, while S. calendulacea and the hybrid produced opposite results. S. trilobata showed fewer spots stained for reactive oxygen species in tissues, with an increase in superoxide dismutase activity. Although S. trilobata is a heliophilous plant, we found that the shade tolerance of S. trilobata and the hybrid were stronger than that of S. calendulacea, which may be one important mechanism of invasion.

Antioxidant Properties of Plastoquinone and Prospects of its Practical Application

This review describes the properties of reactive oxygen species that determine their destructive impact on the tissues of animals and plants and also presents the mechanisms of formation of reactive oxygen species in these tissues. The importance of antioxidant protection of hydrophobic zones, first of all, lipid membranes, in living organisms is underlined. Pathological states initiated by violation of the membrane structure and composition, in particular, due to the toxic effect of cholesterol oxidation products are described; data on such states arising from oxidative processes in low-density lipoproteins are provided. The results of application of ubiquinone and plastoquinone derivatives as membrane antioxidants and regulators of the level of reactive oxygen species in tissues are presented. The advantages of natural plastoquinone as a lipid-soluble compound that protects cell components from oxidation are discussed.

Size dependent oxidative stress response of the gut of Daphnia magna to functionalized nanodiamond particles

Nanodiamonds are a type of engineered nanomaterial with high surface area that is highly tunable and are being proposed for use as a material for medical imaging or drug delivery to composites. With their potential for widespread use they may potentially be released into the aquatic environment as are many chemicals used for these purposes. It is generally thought that nanodiamonds are innocuous, but toxicity may occur due to surface functionalization. This study investigated the potential oxidative stress and antioxidant response of enterocytes in a freshwater invertebrate, Daphnia magna, a common aquatic invertebrate for ecotoxicological studies, in response to two types of functionalized nanodiamonds (polyallylamine and oxidized). We also examined how the size of the nanomaterial may influence toxicity by testing two different sizes (5 nm and 15 nm) of nanodiamonds with the same functionalization. Adults of Daphnia magna were exposed to three concentrations of each of the nanodiamonds for 24 h. We found that both 5 and 15 nm polyallylamine nanodiamond and oxidized nanodiamond induced the production of reactive oxygen species in tissues. The smaller 5 nm nanodiamond induced a significant change in the expression of heat shock protein 70 and glutathione-S-transferase. This may suggest that daphnids mounted an antioxidant response to the oxidative effects of 5 nm nanodiamonds but not the comparative 15 nm nanodiamonds with either surface chemistry. Outcomes of this study reveal that functionalized nanodiamond may cause oxidative stress and may potentially initiate lipid peroxidation of enterocyte cell membranes in freshwater organisms, but the impact of the exposure depends on the particle size.

Rebamipide suppresses mite-induced asthmatic responses in NC/Nga mice.

Allergic asthma caused by continuous allergen exposure evokes allergen-specific Th2 responses and is characterized by chronic airway inflammation and hyperresponsiveness. A previous report showed that rebamipide improved asthmatic symptoms in an ovalbumin/trypsin mice model. However, it is still unclear how rebamipide exerts its effects in asthma. In this study, rebamipide improved the asthmatic responses induced by mite exposure in NC/Nga mice, revealing the mechanism of this therapeutic effect. Rebamipide suppressed the infiltration of eosinophils into the airways and lung as well as attenuating the production of reactive oxygen species in tissues. In addition to these anti-inflammatory effects, rebamipide inhibited the production of IL-33, a member of the IL-1 family that drives the subsequent production of Th2-associated cytokines. These observations identify the point where rebamipide exerts its suppressive action on asthma and suggest that rebamipide has therapeutic potential in preventing mite-induced asthma.

Kynurenines with Neuroactive and Redox Properties: Relevance to Aging and Brain Diseases

The kynurenine pathway (KP) is the main route of tryptophan degradation whose final product is NAD+. The metabolism of tryptophan can be altered in ageing and with neurodegenerative process, leading to decreased biosynthesis of nicotinamide. This fact is very relevant considering that tryptophan is the major source of body stores of the nicotinamide-containing NAD+ coenzymes, which is involved in almost all the bioenergetic and biosynthetic metabolism. Recently, it has been proposed that endogenous tryptophan and its metabolites can interact and/or produce reactive oxygen species in tissues and cells. This subject is of great importance due to the fact that oxidative stress, alterations in KP metabolites, energetic deficit, cell death, and inflammatory events may converge each other to enter into a feedback cycle where each one depends on the other to exert synergistic actions among them. It is worth mentioning that all these factors have been described in aging and in neurodegenerative processes; however, has so far no one established any direct link between alterations in KP and these factors. In this review, we describe each kynurenine remarking their redox properties, their effects in experimental models, their alterations in the aging process.

Temporal Leukocyte Numbers and Granulocyte Activation in Pulsatile and Rotary Ventricular Assist Device Patients

Individual ventricular assist device (VAD) design may affect leukocytes and impact immunity. Few studies have presented leukocyte and infection profiles in VAD patients over the course of the implant period. CD11b (MAC-1) expression on granulocytes is an indicator of activation during inflammation, mediating extravasation and the release of reactive oxygen species in tissue. No reported studies have presented MAC-1 expression on circulating granulocytes in VAD patients. Fifty-six patients implanted at a single center with a HeartMate II (HMII; n = 32), HeartWare (HW; n = 12), or Thoratec pneumatic VAD (PVAD; n = 12) between 1999 and 2011 were followed for 120 days of support. The leukocyte profiles and infectious events of all patients were evaluated; additionally, a subset had MAC-1 expression on circulating granulocytes was measured (HMII n = 9; HW n = 7; PVAD n = 4). All groups exhibited a significant peak in leukocyte numbers at postoperative day (POD) 14 while simultaneously experiencing a significant decrease in hematocrit. HMII patients exhibited a 3.2-fold increase in granulocyte MAC-1 expression at POD 14, and the temporal trend over the implant period differed from that experienced by HW patients. Further, HW patients experienced significantly fewer infection events. Alterations in leukocyte profiles and granulocyte activation experienced by VAD patients appear to be device-specific. Elevations in leukocyte activation may be related to an increased risk for infection, although the specific relationship between these phenomena in this patient group is not known.

Anti-inflammatory and redox-protective activities of citronellal.

The anti-inflammatory and redox protective effects of the citronellal (CT) were evaluated using in vivo and in vitro tests. Intraperitoneal (i.p.) administration of CT (50, 100, and 200 mg/kg) inhibited (p < 0.05) the carrageenan-induced leukocyte migration to the peritoneal cavity. Additionally, the carrageenan- and arachidonic acid-induced rat hind paw edema was significantly inhibited (p < 0.05) by i.p. administration of 100 and 200 mg/kg of the compound. When the redox activity was evaluated, CT (200 mg/kg) significantly reduced hepatic lipoperoxidation (p < 0.001), as well as oxidation of plasmatic (p < 0.05) and hepatic (p < 0.01) proteins. The results of the present study support the hypothesis that CT possesses anti-inflammatory and redox protective activities. It is suggested that its effects are associated with the inhibition of the enzymes in the arachidonic acid pathway, which prevent cell migration by inhibiting leukotriene production, edema formation and the increase of reactive oxygen species in tissues. Therefore, CT is of potential benefit to manage inflammatory disorders and correlated damages caused by oxidant agents.

EPR Method for ex vivo Detection of Reactive Oxygen Species in Tissue

Measurement of free radicals, ex vivo, in biological tissue with continuous wave electron paramagnetic resonance (EPR) has been problematic. Here, a novel EPR spin trapping technique has been developed that places one or two large segments of porcine arterial tissue along with supernatant directly into a standard EPR spectrometer cavity at liquid nitrogen temperature. This approach is validated in porcine arterial tissues treated as controls in vivo. To investigate that this method has lower extraneous ROS generation than methods which slice tissue into thin slivers before assaying for reactive oxygen species (ROS), we take two sets of coronary arterial tissue from the same animal. In the first set, we excise one or two large segments of tissue, and in the second set we section the tissue into ten pieces. In both cases, tissue was harvested, placed in physiological saline solution with 190-mM PBN (N-tert-butyl-α-phenylnitrone) and incubated in the dark for 2 hours at physiological temperature while gently being stirred. Tissue and supernatant were then loaded into a syringe and frozen at minus eighty degrees Celsius until EPR analysis. Although absorption of microwaves by an aqueous sample typically at room temperature limits the size of the sample; this method can accommodate as large as 20-mm3 tissue volume into the EPR cavity at liquid nitrogen temperature. In our experiments the tissue volumes were in a range of values between 2 mm3 and 5 mm3,and the EPR spectra were normalized with respect to tissue volume.

Control of Reactive Oxygen Species Production in Contracting Skeletal Muscle

The increased activities of free radicals or reactive oxygen species in tissues of exercising humans and animals were first reported ∼30 years ago. A great deal has been learned about the processes that can generate these molecules, but there is little agreement on which are important, how they are controlled, and there are virtually no quantitative data. Superoxide and nitric oxide are generated by skeletal muscle and their reactions lead to formation of secondary species. A considerable amount is known about control of superoxide generation by xanthine oxidase activity, but similar information for other generation systems is lacking. Re-evaluation of published data indicates potential approaches to quantification of the hydrogen peroxide concentration in resting and contracting muscle cells. Such calculations reveal that, during contractions, intracellular hydrogen peroxide concentrations in skeletal muscle may only increase by ∼100 nM. The primary effects of this modest increase appear to be in "redox" signaling processes that mediate some of the responses and adaptations of muscle to exercise. These act, in part, to increase the expression of cytoprotective proteins (e.g., heat shock proteins and antioxidant enzymes) that help maintain cell viability. During aging, these redox-mediated adaptations fail and this contributes to age-related loss of skeletal muscle. Understanding the control of ROS generation in muscle and the effect of aging and some disease states will aid design of interventions to maintain muscle mass and function, but is dependent upon development of new analytical approaches. The final part of this review indicates areas where such developments are occurring.

Cardiac and pulmonary oxidative stress in rats exposed to realistic emissions of source aerosols

In vivo chemiluminescence (CL) is a measure of reactive oxygen species in tissues. CL was used to assess pulmonary and cardiac responses to inhaled aerosols derived from aged emissions of three coal-fired power plants in the USA. Sprague–Dawley rats were exposed to either filtered air or: (1) primary emissions (P); (2) ozone oxidized emissions (PO); (3) oxidized emissions + secondary organic aerosol (SOA) (POS); (4) neutralized oxidized emissions + SOA (PONS); and (5) control scenarios: oxidized emissions + SOA in the absence of primary particles (OS), oxidized emissions alone (O), and SOA alone (S). Immediately after 6 hours of exposure, CL in the lung and heart was measured. Tissues were also assayed for thiobarbituric acid reactive substances (TBARS). Exposure to P or PO aerosols led to no changes compared to filtered air in lung or heart CL at any individual plant or when all data were combined. POS caused significant increases in lung CL and TBARS at only one plant, and not in combined data from all plants; PONS resulted in increased lung CL only when data from all plants were combined. Heart CL was also significantly increased with exposure to POS only when data from all plants were combined. PONS increased heart CL significantly in one plant with TBARS accumulation, but not in combined data. Exposure to O, OS, and S had no CL effects. Univariate analyses of individual measured components of the exposure atmospheres did not identify any component associated with increased CL. These data suggest that coal-fired power plant emissions combined with other atmospheric constituents produce limited pulmonary and cardiac oxidative stress.

Anti-inflammatory and redox-protective activities of citronellal

The anti-inflammatory and redox protective effects of the citronellal (CT) were evaluated using in vivo and in vitro tests. Intraperitoneal (i.p.) administration of CT (50, 100, and 200 mg/kg) inhibited (p < 0.05) the carrageenan-induced leukocyte migration to the peritoneal cavity. Additionally, the carrageenan- and arachidonic acid-induced rat hind paw edema was significantly inhibited (p < 0.05) by i.p. administration of 100 and 200 mg/kg of the compound. When the redox activity was evaluated, CT (200 mg/kg) significantly reduced hepatic lipoperoxidation (p < 0.001), as well as oxidation of plasmatic (p < 0.05) and hepatic (p < 0.01) proteins. The results of the present study support the hypothesis that CT possesses anti-inflammatory and redox protective activities. It is suggested that its effects are associated with the inhibition of the enzymes in the arachidonic acid pathway, which prevent cell migration by inhibiting leukotriene production, edema formation and the increase of reactive oxygen species in tissues. Therefore, CT is of potential benefit to manage inflammatory disorders and correlated damages caused by oxidant agents.

Effect of Hyperbaric Oxygen on Cyclosporine-Induced Nephrotoxicity and Oxidative Stress in Rats

Reactive oxygen species have been suggested to be involved in cyclosporine nephrotoxicity. Hyperbaric oxygen is known to induce the generation of reactive oxygen species in tissues. The aim of this study was to investigate whether the use of hyperbaric oxygen concurrently with cyclosporine potentiates cyclosporine nephrotoxicity by inducing oxidative stress in kidneys. The study consisted of four groups of rats: a control group, a cyclosporine group (15 mg/kg/day intraperitoneally for 14 days), a hyperbaric oxygen group (60 min. every day for five days at 2.5 atmosphere absolute), and a cyclosporine + hyperbaric oxygen group (cyclosporine 15 mg/kg/day intraperitoneally for 14 days + hyperbaric oxygen for 60 min at 2.5 atmosphere absolute every day for five days on the last five days of cyclosporine treatment). Oxidative stress was determined by measuring renal thiobarbituric acid-reactive substances content, renal superoxide dismutase, and glutathione peroxidase activities. Cyclosporine increased serum urea and creatinine levels, indicating the development of nephrotoxicity, and induced significant oxidative stress in rat kidneys. Hyperbaric oxygen alone did not alter any of the biochemical and oxidative stress parameters compared to the control group. When used concurrently with cyclosporine, hyperbaric oxygen significantly reduced cyclosporine-induced oxidative stress, but it neither attenuated nor aggravated cyclosporine-induced nephrotoxicity. These results suggest that reactive oxygen species are involved in cyclosporine nephrotoxicity, but are not the direct cause of the toxicity. Although concurrent use of cyclosporine and hyperbaric oxygen did not exacerbate cyclosporine nephrotoxicity in this model, we recommend that the renal functions of patients be monitored periodically when these treatments are used concurrently.

Characterization of Transformed Arabidopsis with Altered Alternative Oxidase Levels and Analysis of Effects on Reactive Oxygen Species in Tissue

The alternative oxidase (AOX) of plant mitochondria transfers electrons from the ubiquinone pool to oxygen without energy conservation. AOX can use reductant in excess of cytochrome pathway capacity, preventing reactive oxygen species (ROS) formation from an over-reduced ubiquinone pool, and thus may be involved in acclimation to oxidative stresses. The AOX connection with mitochondrial ROS has been investigated only in isolated mitochondria and suspension culture cells. To study ROS and AOX in whole plants, transformed lines of Arabidopsis (Arabidopsis thaliana) were generated: AtAOX1a overexpressors, AtAOX1a anti-sense plants, and overexpressors of a mutated, constitutively active AtAOX1a. In the presence of KCN, leaf tissue of either mutant or wild-type AOX overexpressors showed no increase in oxidative damage, whereas anti-sense lines had levels of damage greater than those observed for untransformed leaves. Similarly, ROS production increased markedly in anti-sense and untransformed, but not overexpressor, roots with KCN treatment. Thus, AOX functions in leaves and roots, as in suspension cells, to ameliorate ROS production when the cytochrome pathway is chemically inhibited. However, in contrast with suspension culture cells, no changes in leaf transcript levels of selected electron transport components or oxidative stress-related enzymes were detected under nonlimiting growth conditions, regardless of transformation type. Further, a microarray study using an anti-sense line showed AOX influences outside mitochondria, particularly in chloroplasts and on several carbon metabolism pathways. These results illustrate the value of expanding AOX transformant studies to whole tissues.

Inhibition of inflammation contributes to organ protection of atenolol in sinoaortic-denervated rats.

The present study was designed to test the hypothesis that inhibition of inflammation contributes to the protective effects of atenolol on the organ damage induced by sinoaortic denervation (SAD) in rats. SAD was performed in male Sprague-Dawley rats at the age of 10 weeks. Atenolol (20 mg/kg/d, po) was administered for 12 weeks beginning from 4 weeks after SAD. Organ damage evaluation and the determination of plasma TXB2, serum IL-1, TNF-alpha and tissue reactive oxygen species (ROS) were performed at 16 weeks after SAD. It was found that there existed obvious organ damage including increased cardiac and aortic collagen, and glomerular injury, in SAD rats. Plasma TXB2, serum TNF-alpha IL-1, and tissue ROS increased significantly after SAD. Long-term treatment with atenolol significantly prevented the organ damage with a decrease in left ventricular weight, cardiac and aortic collagen contents, and glomerular injury score in SAD rats. Plasma TXB2, serum IL-1, and tissue ROS were found to be significantly decreased by the long-term treatment with atenolol. Furthermore, it was found that the levels of inflammation-related factors were significantly related to all the organ-damage parameters studied in this experiment. These results suggest that inhibition of inflammation and oxygen stress contributes to the organ-protective effects of atenolol in SAD rats.

A comparative study of superoxide dismutase activity in marine benthic invertebrates with respect to environmental sulphide exposure

Exposure to environmental sulfide has been related to formation of reactive oxygen species (ROS) in vertebrate and invertebrate tissues. The present paper compares activity levels of the oxygen radical quencher superoxide dismutase (SOD) in benthic polychaetes and bivalves of differing sulphide tolerance. Total SOD activity showed no correlation to biotope related sulphide exposure of different species. Sulfide-insensitive MnSOD is present in tissues and body fluids of some sulphide adapted species. Total SOD activity was generally higher in haemoglobin containing animals, than in species lacking respiratory pigments. The sulphide-resistant MnSOD was the dominating enzymatic form in respiratory fluids of haemoglobin containing species, whereas sulphide-sensitive CuZnSOD dominated in the body tissues. Bivalves without respiratory pigments had mostly SOD deficient haemolymph. The results indicate, that release of reactive oxygen species in tissues and body fluids of invertebrates could be connected to the presence of haemoglobin, rather than to sulphide oxidation.

Reactive Oxygen Species Production in the Isolated Perfused Rat Liver: Effect of Respiratory Inhibitors.

Mitochondria are one of the possible sources of potentially harmful reactive oxygen species in tissue during ischemia-reperfusion. In order to delineate the capacity of the respiratory chain to produce reactive oxygen species, the effect of respiratory inhibitors on the oxygen uptake and luminol and lucigenin enhanced chemiluminescence was measured in isolated blood-free perfused rat livers. Concomitant tissue damage was monitored by measuring the release of lactate dehydrogenase and thiobarbituric acid reactive substances by the livers. Cyanide inhibited oxygen uptake reversibly while rotenone and Antimycin A effects were not reversible. Enhanced chemiluminescence was increased immediately by cyanide, suggesting increased formation of reactive oxygen species. Antimycin A produced a delayed, large increase in chemiluminescence concurrent with severe cell damage and increased lipid peroxidation; Cyanide and rotenone induced only limited cell damage. The cell damaging effect of Antimycin A was delayed by the simultaneous administration of cyanide. These results are discussed in terms of the possible role of reactive oxygen species produced during Antimycin A inhibition of the respiratory chain in cell damage.

Mechanisms for the generation of oxygen radicals by drugs.

In this report I will give a brief overview of drug-dependent metabolic reactions that can generate reactive oxygen species in tissues. The term drug is used here in its widest sense and includes any physiologically useless compound, either synthetic or naturally occurring, that can transfer one or two electrons to dioxygen via enzyme-catalyzed reactions. At the molecular level it is an enzyme that recognizes a specific structure and sustains the reaction. Therefore, a discussion of biochemical mechanisms is primarily concerned with the nature of the reaction and the identity of enzymes that catalyze reactions. The following review follows this general plan and focuses on enzymes that catalyze oxidation or reduction of functional groups in xenobiotics that often lead to the generation of oxygen radicals.KeywordsXanthine OxidaseMonoamine OxidaseNicotinamide Adenine Dinucleotide PhosphateAldehyde OxidaseAromatic Nitro CompoundThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.