Oxygen Radical Activity Research Articles

Stroke management in the modern settings

Background. Each 6 seconds 1 person in the world dies of a stroke. The stages of stroke care are the following: case detection, emergency medical care, diagnosis, treatment in the hyperacute and acute period, early and subsequent rehabilitation. The main symptoms of stroke can be identified with the help of FAST system (face – facial asymmetry, arm – limb weakness, speech – blurred speech, time – time after the event).
 Objective. To identify the main features of the management of stroke patients.
 Materials and methods. Analysis of the guidelines and literature data.
 Results and discussion. According to the recommendations of the American Heart Association for the emergency service, the time of processing of the call should be up to 90 seconds, the response time of the emergency service – 8 minutes, and the time spent at the place of care – up to 15 minutes. Upon admission to the hospital, the doctor of the stroke unit collects the anamnesis and takes a brief neurological examination, as well as determines the main physiological parameters. The nurse performs tests, the results of which come during thrombolysis. Then the patient undergoes a computed tomography, first aid is given and thrombolysis begins (still in the tomography apparatus). Time must be constantly documented. The median time should be 25 minutes. To organize the work of the stroke unit in the hyperacute and acute period of stroke it is necessary to create a local protocol – a document that lists the care procedures in a particular institution and describes the responsibility and coordination of individual units, time frames of each stage and basic medical services. It is also necessary to create a clinical roadmap for the patient, which includes a map of his moving, the content of procedures and their timer. Optimization of the stroke management is extremely important, as each 15 minutes of time saved leads to the 4 % reduction in mortality and to the 4 % increase in the likelihood of no adverse effects. In the first 3 hours it is especially important to monitor such parameters as body temperature, blood glucose, swallowing function (fever, sugar, swallowing – FESS) thoroughly. It is a significant problem, but for the most options of medical support the evidence base is insufficient, and therefore the doctor faces the choice to follow imperfect recommendations or to prescribe drugs according to the pathogenesis of cerebral ischemia. This choice has to be made in settings of severe time shortage, because the stroke kills 9,000 neurons every second. Stages of the ischemic cascade include ischemia, glutamate excitotoxicity, mitochondrial damage and dysfunction, oxidative and nitrosative stress, inflammation, and microcirculation disorders. Edaravone affects these stages, reducing the activity of oxygen radicals, the permeability of the blood-brain barrier, and the activity of secondary inflammation. This reduces the ischemic penumbra and the brain tissue necrosis area, which increases the likelihood of functional recovery. The study by M. Enomoto et al. (2019) showed that the use of edaravone and the endovascular reperfusion is a promising strategy for the treatment of ischemic stroke.
 Conclusions. 1. To coordinate the work of the stroke unit in the hyperacute and acute period of stroke, it is necessary to create local protocols and the clinical roadmap. 2. During the first 3 hours it is especially important to monitor such parameters as body temperature, blood glucose, and swallowing function. 3. Edaravone affects the ischemic stroke, reducing the activity of oxygen radicals, the permeability of the blood-brain barrier, and the activity of secondary inflammation.

The effect of intrauterine resuscitation by maternal hyperoxygenation on perinatal and maternal outcome: a randomized controlled trial

Maternal hyperoxygenation is widely used during labor as an intrauterine resuscitation technique. However, robust evidence regarding its beneficial effect and potential side effects is scarce, and previous studies show conflicting results. To assess the effect of maternal hyperoxygenation upon suspected fetal distress during the second stage of term labor on fetal heart rate, neonatal outcome, maternal side effects, and mode of delivery. In a single-center randomized controlled trial in a tertiary hospital in The Netherlands, participants were randomized in case of an intermediary or abnormal fetal heart rate pattern during the second stage of term labor, to receive either conventional care or 100% oxygen at 10 L/min until delivery. The primary outcome was the change in fetal heart rate pattern. Prespecified secondary outcomes were Apgar score, umbilical cord blood gas analysis, neonatal intensive care unit admission, perinatal death, free oxygen radical activity, maternal side effects, and mode of delivery. We performed subgroup analyses for intermediary and abnormal fetal heart rate, and for small for gestational age fetuses. From March 2016 through April 2018, a total of 117 women were included. Fetal heart rate patterns could be analyzed in 71 women. Changes in fetal heart rate (defined as improvement, equal, or deterioration) in favor of maternal hyperoxygenation were significant (odds ratio, 5.7; 95% confidence interval, 1.7-19.1) using ordinal logistic regression. Apgar score, umbilical cord blood gas analysis, free oxygen radicals, and mode of delivery showed no significant differences between the intervention and control group. Among women with an abnormal fetal heart rate, there were fewer episiotomies on fetal indication in the intervention group (25%) than in the control group (65%, P< .01). Maternal hyperoxygenation has a positive effect on the fetal heart rate in the presence of suspected fetal distress during the second stage of labor. There was no significant difference in the mode of delivery or neonatal outcome; however, significantly fewer episiotomies on fetal indication were performed following maternal hyperoxygenation in the subgroup with abnormal fetal heart rate pattern.

Malondialdehyde as a Marker of Oxidative Stress in Periodontitis Patients.

Background:Periodontology is a fast-evolving field with newer insights into traditional periodontal diagnosis. Advances in periodontal disease diagnostic research are moving toward methods whereby periodontal risk can be identified and quantified by objective measures such as biomarkers.Objectives:The aim of this study was to evaluate malondialdehyde (MDA) levels in whole saliva of patients with chronic periodontitis.Materials and Methods:Whole saliva samples were collected from 85 patients: 30 patients with chronic periodontitis, 25 with gingivitis, and 30 periodontally healthy controls. To determine the clinical condition of each subject, the gingival index and clinical attachment level were measured. The salivary MDA levels were determined spectrophotometrically.Results:Higher salivary MDA levels (P < 0.005) were detected in patients with periodontitis compared to the healthy controls. There was no statistically significant difference in the salivary MDA levels between patients with gingivitis and healthy controls.Conclusions:Higher salivary MDA levels seem to reflect increased oxygen radical activity during periodontal inflammation. Thus, MDA can be used as a marker of oxidative stress in patients with periodontitis.

Serum oxygen radical activity and total antioxidation capacity are related with severities of surgical patient with sepsis: Prospective pilot study

PurposeThe purpose of this pilot study was to evaluate the correlation between clinical severity and serum oxygen radical activity (ORA) and total antioxidation capacity (TAC) in critically ill surgical patients with sepsis. Materials and methodsThe prospective observational study was performed in surgical intensive care unit (SICU) patients with intra-abdominal sepsis. Serum ORA and TAC levels were measured using a spectrophotometry-based antioxidant assay machine. Serum selenium and zinc levels and plasma glutamine concentrations were also determined. Sequential organ failure assessment (SOFA) and multiple organ dysfunction (MOD) scores were calculated to evaluate the severity. Blood tests and severity scores were assessed on days 1, 3, and 7 in the SICU. ResultsTwenty-seven patients were included. The mean APACHE II score was 22.4. The in-hospital mortality rate was 14.8%. Serum TAC levels correlated positively with SOFA and MOD scores on SICU days 1, 3 and 7, and serum ORA correlated negatively with SOFA and MOD scores on day 3. Serum zinc and selenium levels were lower than normal throughout the observation period. However, there was no significant relationship in clinical severity. ConclusionsSerum TAC level may be a useful biomarker to predict severity of critically ill surgical patients with sepsis.

Protective Effects of Liquiritin on the Brain of Rats with Alzheimer's Disease.

Alzheimer's disease (AD) is a sort of nerve degenerative disease with clinical manifestation of memory damage and cognitive dysfunction. Its typical pathological change is the abnormal deposition of amyloid-beta (Aβ). In this study, a rat AD model with liquiritin (LQ) interference was established to observe the effects of LQ on the AD rats' behavioural memory and primary hippocampus cells. Liquiritin had the effect of improving the rats' learning and memory ability, enhancing the activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in rats' brain tissues, increasing the antioxidant ability, protecting the primary cultured hippocampal neurons and inhibiting the apoptosis induced by Aβ25-35. The protective effects of LQ can be related to the enhancement of antioxidase activity and clearance of oxygen radicals.

Correlation of the oxygen radical activity and antioxidants and severity in critically ill surgical patients – study protocol

BackgroundSurgical patients who require an emergent operation commonly have severe sepsis or septic shock, followed by high morbidity and mortality rates.Despite advances in treatment however, no predictable markers are available. In severe sepsis, many pathophysiologic mechanisms are involved in progression to organ failure, and oxygen free radical and antioxidants are known to contribute to this process. Oxygen free radical and antioxidants contribute to progression of organ failure in severe sepsis. In fact, oxygen radical activity has been reported to be correlated with disease severity and prognosis in patients with severe sepsis or septic shock. Accordingly, we aim to assess the usefulness of oxygen free radical and antioxidant concentrations to predict the disease severity and mortality in a cohort of critically ill surgical patients.Methods/DesignThis is a prospective observation study including patient demographic characteristics, clinical information, blood sampling/serum oxygen radical activity, serum antioxidant activity, serum antioxidant concentrations (zinc, selenium and glutamate), disease severity scores, outcomes, lengths of stay in intensive care unit, hospital 30-day mortality.

Correlation of the oxygen radical activity and antioxidants and severity in critically ill surgical sepsis patients – preliminary report

Correlation of the oxygen radical activity and antioxidants and severity in critically ill surgical sepsis patients – preliminary report

Correlation of the oxygen radical activity and antioxidants and severity in critically ill surgical patients: preliminary report

In septic patients, the oxygen radical (OR) showed toxic effect to induce inflammation and antioxidant activity could affect organ dysfunction. This study was designed to determine the relationship between antioxidant level and severity of organ dysfunction.

Evaluation of the pulmonary effects of short-term nose-only cigarette smoke exposure in mice

Much is known about the chronic effects of cigarette smoke (CS) on lung function and inflammation and development of chronic obstructive pulmonary disease. However, the underlying pathophysiological mechanisms related to the short-term exposure to CS are not fully understood. Here, we assessed the effect of CS generated by nine consecutive cigarettes per day for four days in a nose-only exposure system on airway resistance measured using forced oscillation technique, lung inflammation and oxidative stress in BALB/c mice. Control mice were exposed to air. Mice exposed to CS showed a significant increase of neutrophils and lymphocytes numbers in bronchoalveolar lavage (BAL). The total protein and endothelin levels in BAL fluid were significantly augmented suggesting an increase of alveolar-capillary barrier permeability. Similarly, airway resistance was significantly increased in the CS group compared with controls. Furthermore, reactive oxygen species and lipid peroxidation levels in lung tissue were significantly increased. The antioxidant activities of reduced glutathione, glutathione S transferase and superoxide dismutase were all significantly increased following CS exposure, indicating that CS could trigger adaptive responses that counterbalance the potentially damaging activity of oxygen radicals induced by CS exposure. In conclusion, our data indicate that short-term nose-only exposure to CS causes lung inflammation and increase of airway resistance mediated at least partly through the oxidative stress.

Comprehensive investigation of Ge–Si bonded interfaces using oxygen radical activation

In this work, we investigate the directly bonded germanium-silicon interfaces to facilitate the development of high quality germanium silicon hetero integration at the wafer scale. X-ray photoelectron spectroscopy data is presented which provides the chemical composition of the germanium surfaces as a function of the hydrophilic bonding reaction at the interface. The bonding process induced long range deformation is detected by synchrotron x-ray topography. The hetero-interface is characterized by measuring forward and reverse current, and by high resolution transmission electron microscopy.

Structural and Electrical Properties of Low Temperature Direct Bonded Germanium to Silicon Wafer for Photodetector Applications

A Ge/Si heterostructure with an ultra-thin transition layer was fabricated at low temperature by direct bonding. In-situ oxygen or nitrogen radical activation was performed after hydrophilic cleaning on both Germanium and Silicon surfaces. The interfacial structure was analyzed by Scanning Acoustic Microscopy (SAM) and High-Resolution Transmission Electron Microscopy (HR-TEM). The samples were diced into mesa structures and electrical properties at different locations were measured in order to characterize the quality of the bonded heterostructure.

Low temperature germanium to silicon direct wafer bonding using free radical exposure

A low temperature germanium (Ge) to silicon (Si) wafer bonding method was demonstrated by in situ radical activation bonding in vacuum. In order to gain further insight into the bonding mechanism, the Ge surface chemistry after either oxygen or nitrogen radical activation was analyzed by means of angle-resolved x-ray photoelectron spectroscopy. After low temperature direct bonding of Ge to Si followed by annealing at 200 and 300 °C, advanced imaging techniques were used to characterize the bonded interface.

Effect of Free Radical Activation for Low Temperature Si to Si Wafer Bonding

In this study, a comparison of different surface treatments for direct Si to Si wafer bonding is reported. Hydrophilic and hydrophobic Si wafers have been exposed to a range of pretreatments, involving oxygen and nitrogen radical activation before in situ wafer bonding in vacuum. After low temperature annealing at 200 and , the formation of voids has been observed by using scanning acoustic microscope inspection. A comparison of the bonding energy has been conducted and analyzed as a function of the surface treatments. Our experiments demonstrate that the remote plasma pretreatment is a very suitable process for surface modification of hydrophilic and hydrophobic Si to Si direct wafer bonding.

Size-dependent effects of tungsten carbide–cobalt particles on oxygen radical production and activation of cell signaling pathways in murine epidermal cells

Hard metal or cemented carbide consists of a mixture of tungsten carbide (WC) (85%) and metallic cobalt (Co) (5–15%). WC–Co is considered to be potentially carcinogenic to humans. However, no comparison of the adverse effects of nano-sized WC–Co particles is available to date. In the present study, we compared the ability of nano- and fine-sized WC–Co particles to form free radicals and propensity to activate the transcription factors, AP-1 and NF-κB, along with stimulation of mitogen-activated protein kinase (MAPK) signaling pathways in a mouse epidermal cell line (JB6 P +). Our results demonstrated that nano-WC–Co generated a higher level of hydroxyl radicals, induced greater oxidative stress, as evidenced by a decrease of GSH levels, and caused faster JB6 P + cell growth/proliferation than observed after exposure of cells to fine WC–Co. In addition, nano-WC–Co activated AP-1 and NF-κB more efficiently in JB6 +/+ cells as compared to fine WC–Co. Experiments using AP-1-luciferase reporter transgenic mice confirmed the activation of AP-1 by nano-WC–Co. Nano- and fine-sized WC–Co particles also stimulated MAPKs, including ERKs, p38, and JNKs with significantly higher potency of nano-WC–Co. Finally, co-incubation of the JB6 +/+ cells with N-acetyl-cysteine decreased AP-1 activation and phosphorylation of ERKs, p38 kinase, and JNKs, thus suggesting that oxidative stress is involved in WC–Co-induced toxicity and AP-1 activation.

Increased Levels of 8-Hydroxydeoxyguanosine and Malondialdehyde and its Relationship with Antioxidant Enzymes in Saliva of Periodontitis Patients

The aim of this study was to evaluate 8-hydroxydeoxyguanosine (8-OHdG) and Malondialdehyde (MDA) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in whole saliva of patients with chronic periodontitis. Moreover, the relationship among the oxidative damage biomarkers, antioxidant enzymes activities and clinical periodontal status were investigated. Whole saliva samples were collected from 30 patients with chronic periodontitis and 30 periodontally healthy control. To determine the clinical condition of each subject, the plaque index, gingival index, clinical attachment level, and probing depth were measured. The salivary 8-OHdG level was measured using the ELISA method. SOD and GPx activities and MDA levels were determined spectrophotometrically. Higher salivary 8-OHdG and MDA levels (P<.001), and lower salivary SOD and GPx activities (P<.05) were detected in periodontitis patients compared to the healthy controls. Additionally, there were significant negative correlations between salivary levels of 8-OHdG and both salivary SOD and GPx activities as well as between salivary levels of MDA and both salivary SOD and GPx activities (P<.001). Higher salivary 8-OHdG and MDA levels and lower salivary antioxidant activities seem to reflect increased oxygen radical activity during periodontal inflammation.

Compromised GCF total antioxidant capacity in periodontitis: cause or effect?

Oxidative stress is implicated in the pathogenesis of periodontitis. The total antioxidant capacity (TAOC) of gingival crevicular fluid volume (GCF) and plasma appears compromised in periodontitis, but it is unclear whether this predisposes to, or results from the inflammatory process. To investigate longitudinal changes in GCF and plasma TAOC following reductions in periodontal inflammation with successful non-surgical therapy. Two longitudinal studies were run in series on non-smokers with chronic periodontitis (CP). Study-1 (n=17) assessed index sites with mild disease; Study-2 (n=18) investigated deep sites. GCF sampling and clinical measures were performed at baseline and 3 months post-therapy. Plasma and GCF TAOC was determined by enhanced chemiluminescence and 32 age/sex-matched periodontally healthy controls were used. Therapy improved clinical outcomes consistent with the literature. There were no differences in plasma TAOC between periodontitis patients (507+/-92 microMTeq) and controls (520+/-100 microMTeq; p=0.57) at baseline, but GCF TAOC was lower (p<0.0001) in CP patients (680+/-371 microMTeq) than controls (1129+/-722 microMTeq). Successful periodontal therapy did not alter plasma TAOC (p=0.56), but GCF TAOC increased (by 449+/-722 microMTeq, p<0.001) to control subject levels (p=0.47) Local total antioxidant capacity in CP appears to reflect increased oxygen radical activity during periodontal inflammation and can be restored to control subject levels by successful non-surgical therapy.

Protective effects of EGCg or GCg, a green tea catechin epimer, against postischemic myocardial dysfunction in guinea-pig hearts

The protective effects of (−)-epigallocatechin-3-gallate (EGCg) or the C-2 epimer, (−)-gallocatechin-3-gallate (GCg), afforded by their antioxidative activity among green tea catechins were investigated in perfused guinea-pig Langendorff hearts subjected to ischemia and reperfusion. The recovery (%) of the left ventricular developed pressure from ischemia by reperfusion was 34.4% in the control, while in the presence of EGCg (3 × 10 − 5 M) or GCg (3 × 10 − 6 M, a more diluted concentration than that of EGCg), it led to a maximal increase of 78.4% or 76.2%, consistent with a significant preservative effect on the tissue level of ATP at the end of ischemia or reperfusion. In the perfused preparation of mitochondria, EGCg (10 − 5 M) inhibited mitochondrial Ca 2+ elevation by changes in the Ca 2+ content or the acidification of perfusate, similarly to findings with cyclosporin A, a well known inhibitor of the mitochondrial permeability transition pore. By in vitro electron paramagnetic resonance (EPR), EGCg or GCg was found to directly quench the activity of active oxygen radicals, with the strongest activity in tea catechins. EGCg or GCg decreased the caspase-3 activity induced apoptosis. Therefore, it is concluded that the beneficial effects of EGCg or GCg play an important role in ischemia–reperfusion hearts in close relation with nitric oxide (NO), active oxygen radicals and biological redox systems in mitochondria.

Maternal and fetal indicators of oxidative stress during intrauterine growth retardation (IUGR)

The present study demonstrates the possibility of increased lipid peroxidation and protein oxidation in both maternal and fetal erythrocytes as markers of oxygen radical activity during intrauterine growth retardation. The erythrocyte MDA levels were significantly elevated in mothers of IUGR babies when compared to controls (p<0.01). The endogenous protein damage due to oxidative stress was significantly higher in IUGR mothers when compared to controls (p<0.05). Similarly the proteolytic activity in erythrocyte lysates against oxidatively damaged hemoglobin was significantly increased in mothers of IUGR babies compared to controls (p<0.001).In fetuses born with IUGR, both lipid peroxidation and proteolytic activity were significantly increased when compared to normal newborns (p<0.01).The result of this study indicates that oxidative stress was induced both in IUGR babies and their mothers which is manifested as increased lipid peroxidation and protein oxidant damage.

Protective effects of some antineoplastic agents on ischemia-reperfusion injury in epigastric island skin flaps

Neutrophil depletion has a beneficial effect on ischemic myocardium and skeletal muscle upon reperfusion. Antineoplastic agents reduce blood neutrophils effectively, and lead to neutrophil depletion. The purpose of this study was to investigate the effects of four antineoplastic agents in low doses (cyclophosphamide, cisplatinum, mitomycin-C, and 5-fluorouracil) on ischemia-reperfusion injury, using an epigastric island skin-flap model in rats. Fifty male Sprague-Dawley rats, weighing 250-300 g, were randomly divided into five groups, each consisting of 10 rats: control, cyclophosphamide, cisplatinum, mitomycin-C, and 5-fluorouracil groups. Epigastric island skin flaps (measuring 3.5 x 4 cm) were raised and subjected to 10 h of in situ ischemia, followed by 7-day reperfusion and evaluation. Treatment with antineoplastic agents (cyclophosphamide, cisplatinum, mitomycin-C, and 5-fluorouracil) was used to introduce neutropenia. Complete blood counts, cutaneous bleeding time, and skin-flap survival were evaluated. Additionally, levels of malonyldialdehyde (MDA), nitric oxide (NO), glutathione (GSH), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) were measured from extracted skin tissue. Numbers of leukocytes and platelets were decreased in all experimental groups. However, neutropenia and thrombocytopenia were not seen. Cutaneous bleeding activity was prolonged in all experimental groups, but not above the normal value. MDA and NO levels were found to be lower in all four antineoplastic agent groups than in the control group, while GSH, GSH-Px, and SOD enzyme activities were significantly higher (P < 0.05). However, MDA and NO levels were significantly decreased in the cyclophosphamide and 5-fluorouracil groups, as compared to the cisplatinum and mitomycin-C groups (P < 0.01). Also, GSH, GSH-Px, and SOD enzyme activities were significantly increased in the cyclophosphamide and 5-fluorouracil groups, compared to the other two antineoplastic agent groups (P < 0.01). We conclude that antineoplastic agents have beneficial effects on ischemia-reperfusion injuries when their doses are carefully adjusted, by decreasing the number of leukocytes and platelets, and altering the activity of free oxygen radicals.

Oxygen Free Radical-Dependent Activation of Extracellular Signal-Regulated Kinase Mediates Apoptosis-Like Cell Death after Traumatic Brain Injury

Mitogen-activated protein kinase (MAPK) cascades are membrane-to-nucleus signaling modules that recently have been implicated as mediators of cellular injury. In this study, we investigated the involvement of the MAP kinase p44/p42 (extracellular signal-regulated kinase [ERK1/2]) in traumatic brain injury (TBI) in rats. There was a strong increase in activated, phosphorylated ERK 1/2 (p-ERK 1/2) protein at 10 min up to 24 h after the injury. Expression of p-ERK occurred in cells identified as neurons, astrocytes, and microglia. Most of the cells expressing p-ERK were TUNEL positive at later time points. Treatment with the MEK inhibitor U0126 or the free radical scavenger S-PBN, both with neuroprotective properties in TBI, attenuated the early activation of ERK and resulted in less activation of caspase-3 and subsequent DNA fragmentation. Post-treatment with U0126 resulted in a significant decrease (-60%) in cortical cavity size and cortical atrophy at 2 weeks after trauma. Overall, the results suggest that ERK activation is initiated by increased oxygen radical activity and that overactivation of ERK sets off secondary cell death mechanisms in TBI. Clinical studies are warranted to evaluate the concept of MEK inhibition in head-injured patients.