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Increased excitotoxity in response to stressors leads to oxidative stress (OS) due to accumulation of excess reactive oxygen/nitrogen species. Neuronal membrane phospholipids are especially susceptible to oxidative damage, which alters signal transduction mechanisms. The Contingent of International Operations (CIO) has been subjected to various extreme stressors that could cause Posttraumatic Stress Disorder (PTSD). Former studies suggest that heterogeneity due to gender, race, age, nutritional condition and variable deployment factors and stressors produce challenges in studying these processes. The research aim was to assess OS levels in the PTSD risk group in CIO. In a prospective study, 143 participants who were Latvian CIO, regular personnel, males, Europeans, average age of 27.4, with the same tasks during the mission, were examined two months before and immediately after a six-month Peace Support Mission (PSM) in Afghanistan. PCL-M questionnaire, valid Latvian language "Military" version was used for PTSD evaluation. Glutathione peroxidase (GPx), superoxide dismutase (SOD) and lipid peroxidation intensity and malondialdehyde (MDA) as OS indicators in blood were determined. Data were processed using SPSS 20.0. The MDA baseline was 2.5582 μM, which after PSM increased by 24.36% (3.1815 μM). The GPx baseline was 8061.98 U/L, which after PSM decreased by 9.35% (7308.31 U/L). The SOD baseline was 1449.20 U/gHB, which after PSM increased by 2.89% (1491.03 U/gHB). The PTSD symptom severity (total PCL-M score) baseline was 22.90 points, which after PSM increased by 14.45% (26.21 points). The PTSD Prevalence rate (PR) baseline was 0.0357, which after PSM increased by 147.06% (0.0882). We conclude that there is positive correlation between increase of OS, PTSD symptoms severity level, and PTSD PR in a group of patients with risk of PTSD - CIO. PTSD PR depends on MDA intensity and OS severity. OS and increased free radical level beyond excitotoxity, is a possible causal factor for clinical manifestation of PTSD

© 2015 The Authors. Published by Frontiers Media. This is an open access article available under a Creative Commons licence. The published version can be accessed at the following link on the publisher's website: https://doi.org/10.3389/fphys.2015.00102 ; Renal failure is accompanied by progressive muscle weakness and premature fatigue, in part linked to hypokinesis and in part to uremic toxicity. These changes are associated with various detrimental biochemical and morphological alterations. All of these pathological parameters are collectively termed uremic myopathy. Various interventions while helpful can't fully remedy the pathological phenotype. Complex mechanisms that stimulate muscle dysfunction in uremia have been proposed, and oxidative stress could be implicated. Skeletal muscles continuously produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) at rest and more so during contraction. The aim of this mini review is to provide an update on recent advances in our understanding of how ROS and RNS generation might contribute to muscle dysfunction in uremia. Thus, a systematic review was conducted searching PubMed and Scopus by using the Cochrane and PRISMA guidelines. While few studies met our criteria their findings are discussed making reference to other available literature data. Oxidative stress can direct muscle cells into a catabolic state and chronic exposure to it leads to wasting. Moreover, redox disturbances can significantly affect force production per se. We conclude that oxidative stress can be in part responsible for some aspects of uremic myopathy. Further research is needed to discern clear mechanisms and to help efforts to counteract muscle weakness and exercise intolerance in uremic patients. ; This work has been co-financed by the European Union (European Social Fund—ESF) and Greek national funds through the Operational Program "Educational and Lifelong Learning" of the National Strategic Reference Framework (NSRF)—Research Funding Program: Thales (MuscleFun Project-MIS 377260) Investing in knowledge society through the European Social Fund. ; Published version

In living organisms, production of reactive oxygen species (ROS) is counterbalanced bytheir elimination and/or prevention of formation which in concert can typically maintain a steadystate (stationary) ROS level. However, this balance may be disturbed and lead to elevated ROSlevels and enhanced damage to biomolecules. Since 1985, when H. Sies first introduced thedefinition of oxidative stress, this area has become one of the hot topics in biology and, to date,many details related to ROS-induced damage to cellular components, ROS-based signaling, cellularresponses and adaptation have been disclosed. However, some basal oxidative damage alwaysoccurs under unstressed conditions, and in many experimental studies it is difficult to showdefinitely that oxidative stress is indeed induced by the stressor. Therefore, usually researchersexperience substantial difficulties in the correct interpretation of oxidative stress development. Forexample, in many cases an increase or decrease in the activity of antioxidant and related enzymesare interpreted as evidences of oxidative stress. Careful selection of specific biomarkers (ROSmodified targets) may be very helpful. To avoid these sorts of problems, I propose severalclassifications of oxidative stress based on its time-course and intensity. The time-courseclassification includes acute and chronic stresses. In the intensity based classification, I propose todiscriminate four zones of function in the relationship between "Dose/concentration of inducer"and the measured "Endpoint": I – basal oxidative stress zone (BOS); II – low intensity oxidativestress (LOS); III – intermediate intensity oxidative stress (IOS); IV – high intensity oxidative stress(HOS). The proposed classifications may be helpful to describe experimental data where oxidativestress is induced and systematize it based on its time course and intensity. Perspective directions ofinvestigations in the field include development of sophisticated classifications of oxidative stresses,accurate identification of cellular ROS targets and their arranged responses to ROS influence, realin situ functions and operation of so-called "antioxidants", intracellular spatiotemporal distributionand effects of ROS, deciphering of molecular mechanisms responsible for cellular response to ROSattacks, and ROS involvement in realization of normal cellular functions in cellular homeostasis.

Over the last few decades, the concentration of cadmium (Cd) in the environment has increased considerably in many countries due to anthropogenic activities. Cd is one of the most toxic pollutants in the environment and affects many metabolic processes in plants. The main objective of this study was to evaluate the response of the production, nutritional, and enzymatic antioxidant system of two tomato genotypes (Calabash Rouge and CNPH 0082) grown in tropical soils that were treated with doses of Cd. Soil samples were collected from the layer of earth at a depth of 0–0.2 m in areas subjected to a minimum of human disturbance. The concentrations of Cd applied to the soil samples were 0, 1, 2, and 4 times (0, 3, 6, and 12 mg kg−1 of Cd) the agricultural intervention value adopted by current environmental legislation in the state of São Paulo, Brazil. Analysis of superoxide dismutase, catalase, glutathione reductase, guaiacol peroxidase, and ascorbate peroxidase activities, formation of stress indicator compound (malondialdehyde—MDA and hydrogen peroxide), parameters of production—dry mass of the shoot and root system (here in after "shoots" and "roots"), as well as nutrition, and both the bioavailable and total levels of this metal in the soil were performed. When the bioavailable content and total levels of Cd in the soil increased as a result of this metal doses applied, the biomass of both shoots and roots decreased in both genotypes (with the exception of the CNPH 0082 grown in clay soil) and displayed lower SPAD (relative chlorophyll index) values when exposed to contaminated environments with Cd concentrations. Cadmium treatment resulted in nutritional imbalances, mainly in terms of N, P, and Mn metabolism. Plants subjected to an elevated available content of metal in the soil exhibited increases in content of MDA and hydrogen peroxide and increased activity of catalase, ascorbate peroxidase, and guaiacol peroxidase in plant tissues when grown in both clay soil and sandy soil. Cadmium was phytotoxic to the plants causing a nutritional imbalance, especially on the metabolisms of N, P, and Mn. An oxidative stress condition was established in response to the Cd treatments applied, which led to changes in peroxidase activity.

The advent of O2 in the atmosphere was among the first major pollution events occurred on earth. The reaction between ferrous iron, very abundant in the reductive early atmosphere, and oxygen results in the formation of harmful superoxide and hydroxyl radicals, which affect all macromolecules (DNA, lipids and proteins). Living organisms have to build up mechanisms to protect themselves against oxidative stress, with enzymes such as catalase and superoxide dismutase, small proteins like thioredoxin and glutaredoxin, and molecules such as glutathione. Bacterial genetic responses to oxidative stress are controlled by two major transcriptional regulators (OxyR and SoxRS). This paper reviews major key points in the generation of reactive oxygen species in bacteria, defense mechanisms and genetic responses to oxidative stress. Special attention is paid to the oxidative damage to proteins. ; Some research work described in this review was supported in part by Grant PB94-0829-C02-02 from DGICYT of the Spanish Government, and by the Comissionat per Universitats i Recerca of the Autonomous Government of Catalonia.

In a few last decades oxidative stress detected in a variety of physiological processeswhere reactive oxygen species (ROS) and reactive nitrogen species (RNS) play a central role. Theyare directly involved in oxidation of proteins, lipids and nucleic acids. In certain concentrationsthey are necessary for cell division, proliferation and apoptosis. Contractile muscle tissue at aerobicconditions form high ROS flow that may modulate a variety of cell functions, for exampleproliferation. However, slight increase in ROS level provide hormetic effect which may participatein adaptation to heavy weight training resulted in hypertrophy and proliferation of skeletal musclefibers. This review will discuss ROS types, sites of generation, strategies to increase forceproduction and achieve skeletal muscle hypertrophy

We hypothesized that increased oxidative stress and disrupted redox balance may be predisposing factors and markers for overreaching (OR). Purpose: To examine whether oxidative stress markers and antioxidant status and physical fitness are related to overreaching during an 8-week military basic training (BT) period. Methods: Oxidative stress and antioxidant status were evaluated in the beginning, after 4 and 7 weeks of training in 35 males (age 19.7 ± 0.3 yrs) at rest and immediately after a 45-min submaximal exercise. Physical activity (PA) was monitored by accelerometer throughout BT. Indicators of OR were also examined. Results: From baseline to wk4 increased daytime moderate to vigorous PA led to concomitant decreases in the ratio oxidized to total glutathione (GSSG/TGSH) and GSSG. After 4 weeks of BT, GSSG/TGSH and GSSG returned to the baseline values at rest, while PA remained unchanged. At every time point acute exercise decreased TGSH and increased GSSG and GSSG/TGSH, while a decrease was observed in antioxidant capacity after 4 weeks of training. In the beginning of BT, OR subjects (11 of the 35 males) had higher GSSG, GSSG/TGSH and malondialdehyde (a marker of lipid peroxidation) at rest (P<0.01-0.05) and lower response of GSSG and GSSG/TGSH ratio (P<0.01) to exercise than noOR subjects. Moreover, OR subjects had higher PA during BT than noOR (P<0.05). Conclusion: The sustained training load during the last four weeks of BT led to oxidative stress observable both at rest and after submaximal exercise. Increased oxidative stress may be a marker of insufficient recovery leading possibly to OR. ; peerReviewed