Production Of Reactive Oxygen Radicals Research Articles

Serum Calprotectin Levels in Vitiligo Patients and Disease Relation

Introduction: Vitiligo is characterized as melanocytes loss in skin and mucous membranes, the pathogenesis of which isn’t yet clarified. Calprotectin is a protein secreted from neutrophils, monocytes, and dendritic cells, which has an effect on cytokine receptor regulation and the production of reactive oxygen radicals. It has been the subject of research in various inflammatory and autoimmune diseases, yet not investigated in vitiligo. Objective: The aim of our study was to investigate the role of calprotectin in the etiopathogenesis of vitiligo and its relationship with clinical subtypes and disease scores. Methods: 44 vitiligo patients with lack of autoimmune disease and 36 age and sex matched healthy controls were involved in the study. Serum calprotectin levels were measured by ELISA. The results were compared with the control group, and the relationship between patients' demographic characteristics, skin phototypes, disease type, disease scores (Vitiligo Area Scoring Index and Vitiligo Disease Activity Score), disease duration, and age at onset were evaluated. Results: The median serum calprotectin level was 454.08 pg/ml (41.19-873.41) in the patient group, and the median serum calprotectin level was 223.17 pg/ml (44.88-1044.43) in the control group. Serum calprotectin level was significantly higher in the patient group than in the control group (p=0.016). No correlation was found between serum calprotectin level and disease scores, disease duration, age, age of onset of disease (p˃0.05).

Septic Cardiomyopathy.

Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis-induced myocardial dysfunction represents reversible myocardial dysfunction which ultimately results in left ventricular dilatation or both, with consequent loss of contractility. Studies on septic cardiomyopathy report a wide range of prevalence ranging from 10% to 70%. Myocardial damage occurs as a result of weakened myocardial circulation, direct myocardial depression, and mitochondrial dysfunction. Mitochondrial dysfunction is the leading problem in the development of septic cardiomyopathy and includes oxidative phosphorylation, production of reactive oxygen radicals, reprogramming of energy metabolism, and mitophagy. Echocardiography provides several possibilities for the diagnosis of septic cardiomyopathy. Systolic and diastolic dysfunction of left ventricular is present in 50-60% of patients with sepsis. Right ventricular dysfunction is present in 50-55% of cases, while isolated right ventricular dysfunction is present in 47% of cases. Left ventricle (LV) diastolic dysfunction is very common in septic shock, and it represents an early biomarker, it has prognostic significance. Right ventricular dysfunction associated with sepsis patients with worse early prognosis. Global longitudinal stress and magnetic resonance imaging (MRI) of the heart are sufficiently sensitive methods, but at the same time MRI of the heart is difficult to access in intensive care units, especially when dealing with critically ill patients. Previous research has identified two biomarkers as a result of the integrated mitochondrial response to stress, and these are fibroblast growth factor-21 (FGF-21) and growth differentiation factor-15 (GDF-15). Both of the mentioned biomarkers can be easily quantified in serum or plasma, but they are difficult to be specific in patients with multiple comorbidities. Mitochondrial dysfunction is also associated with reduced levels of miRNA (microRNA), some research showed significance of miRNA in sepsis-induced myocardial dysfunction, but further research is needed to determine the clinical significance of these molecules in septic cardiomyopathy. Therapeutic options in the treatment of septic cardiomyopathy are not specific, and include the optimization of hemodynamic parameters and the use of antibiotic thera-pies with targeted action. Future research aims to find mechanisms of targeted action on the initial mechanisms of the development of septic cardiomyopathy.

Preparation of Co dual atomic site catalysts loaded on defect-engineered MOFs material with superb chemiluminescent enhancement effect for sensitive detection of bacteria

BackgroundDual atomic site catalysts (DASCs) have aroused extensive interest in analytical chemistry on account of the superb catalytic activity caused by the highly-exposed active centers and synergistic effect of adjacent active centers. The reported protocols for preparing DASCs usually involve harsh conditions such as acid/base etching and high-temperature calcination, leading to unfavorable water dispersity and restricted application. It is crucial to develop DASCs with satisfactory water dispersity, improved stability, and mild preparation procedures to facilitate their application as signal probes in analytical chemistry. Results: Formic acid was adopted as a modulator for preparing MOF-808 with abundant defective sites, which was used as the carrier for implanting Co atoms. Co DASCs with a special coordination structure of Co2–O10 and a high loading efficiency of 11.1 wt% were prepared with a mild solvothermal protocol. The resultant Co DASCs can significantly accelerate decay of H2O2 for forming numerous reactive oxygen radicals and boost chemiluminescent (CL) signal. Co DASCs at 1.0 μg mL−1 can enhance the CL signal of luminol-H2O2 system by about 5800 times. Thanks to their satisfactory water dispersity and excellent CL enhancement performance, they were used as ultra-sensitive CL signal probes for monitoring methicillin-resistant Staphylococcus aureus. The method shows a detection range of 102–107 CFU mL−1 and a detection limit of 47 CFU mL−1. Antibiotic susceptibility test was performed with the established CL method to prove its practicality. Significance: The water dispersible Co DASCs prepared with facile and mild solvothermal protocol exhibit prominent peroxidase-like activity and can promote the production of reactive oxygen radicals for boosting CL signal. Therefore, this study paves an avenue for implanting DASCs in defect-engineered carrier to prepare signal probes suitable for development of ultra-sensitive CL analytical methods.

Green synthesis of silver nanoparticles, graphene, and silver-graphene nanocomposite using Melissa officinalis ethanolic extract: Anticancer effect on MCF-7 cell line.

Nanotechnology has helped a lot in diagnosing and treating multiple illnesses, specifically cancer, and increasing the development of targeted drug delivery methods. Nanocomposites are materials with at least one component smaller than 100 nm. Therefore, this study aims to assess the anticancer effects of silver-graphene nanocomposite on MCF-7. In this study, the rate of inhibition of cancer cell growth and production of reactive oxygen radicals, malondialdehyde, and glutathione stores in MCF7 cells were investigated. Cancer cells were exposed to nano particles for 48 hr. Silver nanoparticles and graphene both reduced the growth rate of MCF-7. Subsequently, by treating the cells with silver-graphene nanocomposite, the rate of inhibition of cell growth at the highest concentration was 84.60%. Nanoparticles also inhibited the growth of cancer cells through the oxidative stress pathway by increasing the amount of intracellular ROS, followed by increasing malondialdehyde and decreasing glutathione stores, so that at the highest combined concentration of nanoparticles, the amounts of LPO and ROS increased up to 70% and 74 %, and glutathione reserves decreased by 16%. Treatment of MCF-7 cells with silver or graphene nanoparticles and combination treatment with these two substances against cisplatin have sound effects, and by affecting oxidative stress factors, such as increased ROS and subsequent increase in lipid membrane damage, inhibit cell growth and proliferation. According to the mathematical model, silver graphene nanocomposite> silver nanoparticles> graphene has the best effect in inhibiting the growth of cancer cells, respectively.

Oxidative Stress as a Potential Mechanism Underlying Membrane Hyperexcitability in Neurodegenerative Diseases.

Neurodegenerative diseases are characterized by gradually progressive, selective loss of anatomically or physiologically related neuronal systems that produce brain damage from which there is no recovery. Despite the differences in clinical manifestations and neuronal vulnerability, the pathological processes appear to be similar, suggesting common neurodegenerative pathways. It is well known that oxidative stress and the production of reactive oxygen radicals plays a key role in neuronal cell damage. It has been proposed that this stress, among other mechanisms, could contribute to neuronal degeneration and might be one of the factors triggering the development of these pathologies. Another common feature in most neurodegenerative diseases is neuron hyperexcitability, an aberrant electrical activity. This review, focusing mainly on primary motor cortex pyramidal neurons, critically evaluates the idea that oxidative stress and inflammation may be involved in neurodegeneration via their capacity to increase membrane excitability.

Can thiol-disulfide balance be an indicator of oxidative stress for hyperhidrosis?

Hyperhidrosis is responsible for various causes. The increased reactive oxygen radical production with insufficient antioxidant mechanism capacity may play a role in the etiopathogenesis of hyperhidrosis. It is probable to gather data about oxidative stress by detecting plasma thiol/disulfide ratio. The aim of this study was to determine whether thiol-disulfide balance changes in patients with hyperhidrosis. The files of patients who were diagnosed with hyperhidrosis in the dermatology outpatient clinic between 2015 and 2018 and whose native thiol, total thiol, and disulfide values were examined for any reason were examined. Seventy-three patients were included in the study. 33 of the patients with hyperhidrosis were primary. Mean age; for primary hyperhidrosis patients (PHH)=26.36±7.61, primary hyperhidrosis (PHH) control group=27.16±7.94; secondary hyperhidrosis (SHH) patients=47.88±12.29, SHH control (45.40±12.02). The native thiol values of PHH (469.93±56.82μmol/L) were higher than SHH (440.64±62.72) (p=0.024). However, as a result of thiol-disulfide comparison between hyperhidrosis patients (PHH and SHH) and control groups, disulfide levels increased (p=0.04). In the PHH group, total thiol was measured as 512±54.84μmol/L, and SHH was measured as 484.11±58.9μmol/L, (p=0.074). Serum thiol levels in SHH increased more than PHH. As a result of thiol-disulfide comparison between hyperhidrosis patients and control groups, the balance shifted in favor of disulfide and oxidative side.

Effect of Sunitinib on Liver Oxidative and Proinflammatory Damage Induced by Ischemia-Reperfusion in Rats

Ischemia-reperfusion (IR) injury is defined as a complex pathologic process that begins with the oxygen deprivation of tissue, continues with the production of reactive oxygen radicals (ROS), and expands with an inflammatory response. This study investigates the protective effects of sunitinib, an anticancer drug with demonstrated antioxidant and anti-inflammatory activity, against liver IR damage. Our study aims to investigate the biochemical and histopathologic effects of sunitinib on IR-induced liver damage in rats. Albino Wistar male rats were divided into 3 groups: liver IR control (IR), 25 mg/kg sunitinib+liver IR (S+IR), and sham operation (SHAM). In the liver tissue of the IR group, oxidant and proinflammatory cytokine levels such as malondialdehyde, nuclear factor κ B, tumor necrosis factor-α, and interleukin-1β increased compared with the SHAM and S+IR groups. In addition, antioxidant levels such as total glutathione, glutathione reductase, and glutathione peroxidase were found to be significantly lower in the IR group than in the SHAM and S+IR groups. Although severe histopathologic damage was observed in the IR group, it was evaluated as mild in the S+IR group. The results obtained suggest that sunitinib may be helpful in the treatment of liver IR injury.

Bioengineering CXCR4-overexpressing cell membrane functionalized ROS-responsive nanotherapeutics for targeting cerebral ischemia-reperfusion injury.

Rationale: As a potentially life-threatening disorder, cerebral ischemia-reperfusion (I/R) injury is associated with significantly high mortality, especially the irreversible brain tissue damage associated with increased reactive oxygen radical production and excessive inflammation. Currently, the insufficiency of targeted drug delivery and “on-demand” drug release remain the greatest challenges for cerebral I/R injury therapy. Bioengineered cell membrane-based nanotherapeutics mimic and enhance natural membrane functions and represent a potentially promising approach, relying on selective interactions between receptors and chemokines and increase nanomedicine delivery efficiency into the target tissues.Methods: We employed a systematic method to synthesize biomimetic smart nanoparticles. The CXCR4-overexpressing primary mouse thoracic aorta endothelial cell (PMTAEC) membranes and RAPA@HOP were extruded through a 200 nm polycarbonate porous membrane using a mini-extruder to harvest the RAPA@BMHOP. The bioengineered CXCR4-overexpressing cell membrane-functionalized ROS-responsive nanotherapeutics, loaded with rapamycin (RAPA), were fabricated to enhance the targeted delivery to lesions with pathological overexpression of SDF-1.Results: RAPA@BMHOP exhibited a three-fold higher rate of target delivery efficacy via the CXCR4/SDF-1 axis than its non-targeting counterpart in an in vivo model. Additionally, in response to the excessive pathological ROS, nanotherapeutics could be degraded to promote “on-demand” cargo release and balance the ROS level by p-hydroxy-benzyl alcohol degradation, thereby scavenging excessive ROS and suppressing the free radical-induced focal damage and local inflammation. Also, the stealth effect of cell membrane coating functionalization on the surface resulted in extended circulation time and high stability of nanoparticles.Conclusion: The biomimetic smart nanotherapeutics with active targeting, developed in this study, significantly improved the therapeutic efficacy and biosafety profiles. Thus, these nanoparticles could be a candidate for efficient therapy of cerebral I/R injury.

Irisin Mitigates Oxidative Stress, Chondrocyte Dysfunction and Osteoarthritis Development through Regulating Mitochondrial Integrity and Autophagy.

Compromised autophagy and mitochondrial dysfunction downregulate chondrocytic activity, accelerating the development of osteoarthritis (OA). Irisin, a cleaved form of fibronectin type III domain containing 5 (FNDC5), regulates bone turnover and muscle homeostasis. Little is known about the effect of Irisin on chondrocytes and the development of osteoarthritis. This study revealed that human osteoarthritic articular chondrocytes express decreased level of FNDC5 and autophagosome marker LC3-II but upregulated levels of oxidative DNA damage marker 8-hydroxydeoxyguanosine (8-OHdG) and apoptosis. Intra-articular administration of Irisin further alleviated symptoms of medial meniscus destabilization, like cartilage erosion and synovitis, while improved the gait profiles of the injured legs. Irisin treatment upregulated autophagy, 8-OHdG and apoptosis in chondrocytes of the injured cartilage. In vitro, Irisin improved IL-1β-mediated growth inhibition, loss of specific cartilage markers and glycosaminoglycan production by chondrocytes. Irisin also reversed Sirt3 and UCP-1 pathways, thereby improving mitochondrial membrane potential, ATP production, and catalase to attenuated IL-1β-mediated reactive oxygen radical production, mitochondrial fusion, mitophagy, and autophagosome formation. Taken together, FNDC5 loss in chondrocytes is correlated with human knee OA. Irisin repressed inflammation-mediated oxidative stress and extracellular matrix underproduction through retaining mitochondrial biogenesis, dynamics and autophagic program. Our analyses shed new light on the chondroprotective actions of this myokine, and highlight the remedial effects of Irisin on OA development.

Energy-transfer-mediated oxygen activation in carbonyl functionalized carbon nitride nanosheets for high-efficient photocatalytic water disinfection and organic pollutants degradation

Polymeric photocatalysts are promising candidates for water purification, however their catalytic performance are still unsatisfactory due to the fast charge recombination that leads to low reactive oxygen radicals production. In this study, a conceptual energy-transfer-mediated photocatalytic oxygen activation system over polymeric carbon nitride without the need of electron-hole separation is proposed, exhibiting remarkable singlet oxygen triggered bacteria inactivation performance as well as organic pollutants degradation. By structure and excitonic effect modulation, the oxygen activation process changes from the traditional electron-transfer mechanism to the final energy-transfer pathway, leading to the selective generation of singlet oxygen with high efficiency. The generated singlet oxygen is found to fervently attack the bacteria membrane, creating irreparable pores or holes on the cell membrane for cytoplasmic contents leaking out to accelerate bacteria destruction. The work demonstrated here offers a new photocatalytic oxygen activation pathway for achieving high-efficient reactive oxygen species generation performance without the need of charge separation.

Size-dependent antibacterial activity of copper nanoparticles against Xanthomonas oryzae pv. oryzae – A synthetic and mechanistic approach

Xanthomonas oryzae pv. oryzae (X. oryzae), causing devastating bacterial leaf blight (BLB) disease in rice, is fast developing resistance against many available antibiotics, warranting an urgent need to develop an alternative control strategy. In this manuscript, we report copper nanoparticles (CuNPs) as an effective antibacterial agent against X. oryzae. We synthesized four different sized CuNPs in a narrow-size range (CuNP-1 – 18 nm, CuNP-2 – 24 nm, CuNP-3 – 28 nm and CuNP-4 – 33 nm) by chemical reduction method. The physicochemical characterizations of CuNPs were done by X-ray diffraction (XRD), dynamic light scattering (DLS), UV–Visible Spectroscopy (UV–Vis Spectroscopy) and transmission electron microscopy (TEM). The antibacterial activity of the CuNPs was found to be size and concentration dependent. Among all the CuNPs, CuNP-3 exerted the best antibacterial efficiency against X. oryzae due to the increased production of reactive oxygen radicals than the others. It also displayed increased activity compared to commercial antibiotic streptomycin sulphate.

Blood biomarkers of nicotine-induced toxicity in healthy males

BackgroundSmoking enhances oxidative stress by causing an oxidant/antioxidant imbalance in the body leading to deleterious effects on various tissues and organs. 8-hydroxy-2′-deoxyguanosine (8-OHdG) is a predominant form of free radical-induced oxidative lesions, and is widely used as a biomarker of oxidative stress.ObjectivesThis study aimed to estimate blood 8-OHdG level in active, passive and non-smokers and its relation with some lifestyle determinants as well as to assess smoking effects on oxidant/antioxidant status.Participants and methodsThe current work included 90 male participants who were classified into 3 groups; 20 non-smokers, 30 passive smokers, and 40 active smokers. Data were collected by answering a premade questionnaire. Peripheral venous blood samples were withdrawn then 8-OHdG, cotinine, superoxide dismutase (SOD), and total antioxidant capacity (TAC) levels were estimated in plasma using ELISA kits, while malondialdehyde (MDA) was estimated by colorimetry.ResultsThere were highly statistically significant higher levels of 8-OHdG, cotinine and MDA and lower levels of SOD and TAC in active smokers compared to both passive and non-smokers (p < 0.001) whereas, no statistically significant difference between passive and non-smokers was detected (p > 0.05). There were no significant differences between 8-OHdG level and smoking habits, age, exercise, tea and coffee consumption, and body mass index (BMI) among the 3 studied groups.ConclusionSmoking induces oxidative stress not only through the production of reactive oxygen radicals and increasing blood 8-OHdG levels but also through weakening of the antioxidant defense systems. Further studies are required to reach a consensus on the background level of 8-OHdG and understand which factors determine it and to further differentiate between passive and non-smokers.

Oxidized Mutant Human Hemoglobins S and E Induce Oxidative Stress and Bioenergetic Dysfunction in Human Pulmonary Endothelial Cells.

Cell free hemoglobin (Hb), becomes oxidized in the circulation during hemolytic episodes in sickle cell disease (SCD) or thalassemia and may potentially cause major complications that are damaging to the vascular system. Hemolytic anemias are commonly associated with pulmonary hypertension (PH) and often result from dysfunction of lung endothelial cells. The aim of this study was to determine the effect of different Hbs on cultured human lung endothelial function. Toward this goal, endothelial permeability, oxidative stress response parameters, glycolytic and mitochondrial bioenergetic functions were monitored in cultured human pulmonary arterial endothelial cells (HPAEC) following incubation with human adult Hb (HbA), and Hb isolated from patients with sickle cell Hb (HbS, βV6E) and HbE (βE26K) that commonly co-exist with β-thalassemia. These mutant Hbs are known for their distinct oxidative profiles. HPAEC treated with the ferrous forms of HbE, HbS for 24 h showed higher loss of endothelial monolayer integrity with concomitant rise in reactive oxygen radical production, lipid hydroperoxide formation and higher expressions of oxidative stress response proteins including heme oxygenase-1 (HO-1) accompanied by a rise in uncoupled mitochondrial respiration. Loss of membrane permeability was diminished in part by haptoglobin (Hp, protein scavenger), hemopexin (Hpx, heme scavenger) or ascorbate (reducing agent). To understand the role of Hb oxidation, HPAEC were exposed to ferric or ferryl states of the mutant Hbs. Ferryl forms of all proteins caused a significant damage to the endothelial monolayer integrity at a higher degree than their respective ferric Hbs. Ferryl forms of HbS and HbE also caused a loss of respiratory chain complex activities in isolated endothelial mitochondria and basal oxygen consumption in HPAEC. However, longer incubation with ferryl Hbs produced bioenergetic reprogramming including higher degree of uncoupled respiration and glycolytic rate. The data in this report collectively indicate that higher oxidation forms of HbS and HbE cause endothelial dysfunction through distinct damaging mechanisms involving mitochondrial bioenergetic function.

Carbon Nitride Supramolecular Hybrid Material Enabled High-Efficiency Photocatalytic Water Treatments.

Surface defects in relation to surface compositions, morphology, and active sites play crucial roles in photocatalytic activity of graphitic carbon nitride (g-C3N4) material for highly reactive oxygen radicals production. Here, we report a high-efficiency carbon nitride supramolecular hybrid material prepared by patching the surface defects with inorganic clusters. Fe (III) {PO4[WO(O2)2]4} clusters have been noncovalently integrated on surface of g-C3N4, where the surface defects provide accommodation sites for these clusters and driving forces for self-assembly. During photocatalytic process, the activity of supramolecular hybrid is 1.53 times than pure g-C3N4 for the degradation of Rhodamine B (RhB) and 2.26 times for Methyl Orange (MO) under the simulated solar light. Under the mediation of H2O2 (50 mmol L-1), the activity increases to 6.52 times for RhB and 28.3 times for MO. The solid cluster active sites with high specific surface area (SSA) defect surface promoting the kinetics of hydroxide radicals production give rise to the extremely high photocatalytic activity. It exhibits recyclable capability and works in large-scale demonstration under the natural sunlight as well and interestingly the environmental temperature has little effects on the photocatalytic activity.

Time and dose dependent effects of oxidative stress induced by cumene hydroperoxide in neuronal excitability of rat motor cortex neurons

It has been claimed that oxidative stress and the production of reactive oxygen radicals can contribute to neuron degeneration and might be one factor in the development of different neurological diseases. In our study, we have attempted to clarify how oxidative damage induces dose dependent changes in functional membrane properties of neurons by means of whole cell patch clamp techniques in brain slices from young adult rats. Our research demonstrates physiological changes in membrane properties of pyramidal motor cortex neurons exposed to 3 concentrations of cumene hydroperoxide (CH; 1, 10 and 100μM) during 30min. Results show that oxidative stress induced by CH evokes important changes, in a concentration and time dependent manner, in the neuronal excitability of motor cortex neurons of the rat: (i) Low concentration of the drug (1μM) already blocks inward rectifications (sag) and decreases action potential amplitude and gain, a drug concentration which has no effects on other neuronal populations, (ii) 10μM of CH depresses the excitability of pyramidal motor cortex neurons by decreasing input resistance, amplitude of the action potential, and gain and maximum frequency of the repetitive firing discharge, and (iii) 100μM completely blocks the capability to produce repetitive discharge of action potentials in all cells. Both larger drug concentrations and/or longer times of exposure to CH narrow the current working range. This happens because of the increase in the rheobase, and the reduction of the cancelation current. The effects caused by oxidative stress, including those produced by the level of lipid peroxidation, are practically irreversible and, this, therefore, indicates that neuroprotective agents should be administered at the first symptoms of alterations to membrane properties. In fact, the pre-treatment with melatonin, acting as an antioxidant, prevented the lipid peroxidation and the physiological changes induced by CH. Larger cells (as estimated by their cell capacitance) were also more susceptible to oxidative stress. Our results provide previously unavailable observations that large size and high sensitivity to oxidative stress (even at low concentrations) make pyramidal neurons of the motor cortex, in particular corticofugal neurons, more susceptible to cell death when compared with other neuronal populations. These results could also shed some light on explaining the causes behind diseases such as Amyotrophic Lateral Sclerosis.

Protective effects of beta glucan in brain tissues of post-menopausal rats: a histochemical and ultra-structural study

Decline of estrogen during menopause has been associated with numerous significant changes that have been linked to many pathophysiological complications. In addition, ovarian hormone deficiency increases the production of reactive oxygen radicals which could result in oxidative stress and cell damage. While estrogen therapy is often considered to overcome the behavioral and physiological shortcomings, antioxidants are gaining popularity for their beneficial property. For this purpose, in the present study, utilizing the antioxidant properties of beta glucan has been examined in treatment of menopause induced oxidative stress in cerebral neurons. Four groups of female Wistar rats were used: control, ovariectomy, ovariectomy + estrogen treated and ovariectomy + beta glucan treated. We observed a significant increase in neural degeneration in ovariectomized rats as compared to controls. Moreover, increased oxidative stress in the brains of the ovariectomized rats has been detected by performing immunohistochemical analysis. A large number of immuno-positive cerebral neurons have been observed in ovariectomy group rat brains. Interestingly, providing beta glucan treatment to ovariectomized rats reduced the number of degenerated neurons. Our study is the first to examine light and electron microscopic examination and immunohistochemical and stereological analysis of estrogen depletion in rats and to test protective role of beta glucan in the experimental study.

Studying the processes of free-radical oxidation in patients with purulent-inflammatory diseases of soft tissues

Aim. To study the effects of combined dressings on the processes of free radical oxidation in patients with purulent wounds.Methods. The performance of luminol-dependent chemiluminescence of whole blood from 30 healthy donors and 122 patients with purulent wounds, as well as tissue chemiluminescence of festering wounds tissue homogenates were examined before and after the treatment. To assess the free radical oxidation in vitro, spontaneous and zymosan-induced whole blood chemiluminescence measurement, iron-induced chemiluminescence assessment of festering wounds tissue homogenates were performed. The distribution of chemiluminescence parameters compared to normal expected distribution was analyzed to group homogeneity on these criteria.Results. Group of donors was homogeneous in composition that allowed the calculation of mean values. By changing in whole blood chemiluminescence of patients with soft tissue festering wounds, they were allocated to two groups, in which a marked increase or decline of the investigated parameters was seen. Increased luminol-dependent blood chemiluminescence indicates excessive free radicals generation by phagocytes and is characteristic of acute inflammation. Decreased intensity of chemiluminescence was observed in the blood of patients who showed reduced functional activity of phagocytes, which, together with the clinical features indicate a long-term smoldering inflammation. The comparative assessment of «Poliderm», «Voskopran», «Polysorb», «Levomekol» medications, used for local treatment of suppurative wounds, influence on free radical oxidation in model systems in vitro, was performed.Conclusion. There is a triple increase in chemiluminescence intensity in the acute phase of the inflammatory process, marking increased production of reactive oxygen radicals with microbicide activity); in long-term smoldering processes, chemiluminescence decreases by half, indicating reduced efficiency of protective mechanisms

Oxidative stress induced by cumene hydroperoxide evokes changes in neuronal excitability of rat motor cortex neurons

Oxidative stress and the production of reactive oxygen radicals play a key role in neuronal cell damage. This paper describes an in vitro study that explores the neuronal responses to oxidative stress focusing on changes in neuronal excitability and functional membrane properties. This study was carried out in pyramidal cells of the motor cortex by applying whole-cell patch-clamp techniques on brain slices from young adult rats. Oxygen-derived free radical formation was induced by bath application of 10μM cumene hydroperoxide (CH) for 30min. CH produced marked changes in the electrophysiological properties of neurons (n=30). Resting membrane potential became progressively depolarized, as well as depolarization voltage, with no variations in voltage threshold. Membrane resistance showed a biphasic behavior, increasing after 5min of drug exposure and then it started to decrease, even under control values, after 15 and 30min. At the same time, changes in membrane resistance produced compensatory variations in the rheobase. The amplitude of the action potentials diminished and the duration increased progressively over time. Some of the neurons under study also lost their ability to discharge action potentials in a repetitive way. Most of the neurons, however, kept their repetitive discharge even though their maximum frequency and gain decreased. Furthermore, cancelation of the repetitive firing discharge took place at intensities that decreased with time of exposure to CH, which resulted in a narrower working range. We can conclude that oxidative stress compromises both neuronal excitability and the capability of generating action potentials, and so this type of neuronal functional failure could precede the neuronal death characteristics of many neurodegenerative diseases.

The effects of salt stress on the germination and antioxidative enzyme activityof Hungarian vetch (Vicia pannonicaCrantz.) varieties

Among abiotic stresses, salinity is one of the most important affecting agricultural production world-wide. In this study, 5 different salt (NaCl) concentrations (0, 50, 100, 150 and, 200 mM) were investigated on the germination and antioxidative enzyme activity of Hungarian vetch seeds. The germination rates, shoot and root lengths, shoot and root fresh weights, shoot/root ratios, lipid peroxidation (MDA), superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and glutathione reductase (GR) activities were evaluated and analyzed at 15 days after placing the seeds in petri dishes. The results indicated a significant variation in the germination and early seedling growth characteristic responses of the varieties to NaCl salinity. It was seen that increasing the NaCl concentration resulted in a decrease in the early seedling growth characteristic germination rates and values of all of varieties used in experiment. However, these decreased less in the tolerant varieties than in the sensitive ones. Under stress conditions, the tolerant varieties showed less of an increase in MDA and more of an increase in SOD, CAT, APX, and GR than the intolerant varieties, indicating that saline stress induces the production of reactive oxygen radicals, resulting in an increase MDA and oxidative stress in the varieties. In Hungarian vetch, this increase in the antioxidant enzyme activities is associated with salt stress tolerance. These results might be beneficial in breeding programs relevant to salinity stress resistance.

Structures and metal-binding properties of Helicobacter pylori neutrophil-activating protein with a di-nuclear ferroxidase center.

Helicobacter pylori causes severe diseases, such as chronic gastritis, peptic ulcers, and stomach cancers. H. pylori neutrophil-activating protein (HP-NAP) is an iron storage protein that forms a dodecameric shell, promotes the adhesion of neutrophils to endothelial cells, and induces the production of reactive oxygen radicals. HP-NAP belongs to the DNA-protecting proteins under starved conditions (Dps) family, which has significant structural similarities to the dodecameric ferritin family. The crystal structures of the apo form and metal-ion bound forms, such as iron, zinc, and cadmium, of HP-NAP have been determined. This review focused on the structures and metal-binding properties of HP-NAP. These metal ions bind at the di-nuclear ferroxidase center (FOC) by different coordinating patterns. In comparison with the apo structure, metal loading causes a series of conformational changes in conserved residues among HP-NAP and Dps proteins (Trp26, Asp52, and Glu56) at the FOC. HP-NAP forms a spherical dodecamer with 23 symmetry including two kinds of pores. Metal ions have been identified around one of the pores; therefore, the negatively-charged pore is suitable for the passage of metal ions.