Reactive Oxygen Species

Abiotic stresses, especially salinity and drought, are the primary causes of crop loss worldwide. Plant adaptation to environmental stresses is dependent upon the activation of cascades of molecular networks involved in stress perception, signal transduction, and the expression of specific stressrelated genes and metabolites. Consequently, engineering genes that protect and maintain the function and structure of cellular components can enhance tolerance to stress. Our limited knowledge of stress-associated metabolism remains a major gap in our understanding; therefore, comprehensive profiling of stress-associated metabolites is most relevant to the successful molecular breeding of stress-tolerant crop plants. Unraveling additional stress-associated gene resources, from both crop plants and highly salt-and droughttolerant model plants, will enable future molecular dissection of salt-tolerance mechanisms in important crop plants.

In a previous communication, we reported a new method of synthesis of stable metallic copper nanoparticles (Cu-NPs), which had high potency for bacterial cell filamentation and cell killing. The present study deals with the mechanism of filament formation and antibacterial roles of Cu-NPs in E. coli cells. Our results demonstrate that NP-mediated dissipation of cell membrane potential was the probable reason for the formation of cell filaments. On the other hand, Cu-NPs were found to cause multiple toxic effects such as generation of reactive oxygen species, lipid peroxidation, protein oxidation and DNA degradation in E. coli cells. In vitro interaction between plasmid pUC19 DNA and Cu-NPs showed that the degradation of DNA was highly inhibited in the presence of the divalent metal ion chelator EDTA, which indicated a positive role of Cu 2+ ions in the degradation process. Moreover, the fast destabilization, i.e. the reduction in size, of NPs in the presence of EDTA led us to propose that the nascent Cu ions liberated from the NP surface were responsible for higher reactivity of the Cu-NPs than the equivalent amount of its precursor CuCl 2 ; the nascent ions were generated from the oxidation of metallic NPs when they were in the vicinity of agents, namely cells, biomolecules or medium components, to be reduced simultaneously.

Reactive oxygen species (ROS) and mitochondria play an important role in apoptosis induction under both physiologic and pathologic conditions. Interestingly, mitochondria are both source and target of ROS. Cytochrome c release from mitochondria, that triggers caspase activation, appears to be largely mediated by direct or indirect ROS action. On the other hand, ROS have also anti-apoptotic effects. This review focuses on the role of ROS in the regulation of apoptosis, especially in inflammatory cells.

Oxygen-free radicals, more generally known as reactive oxygen species (ROS) along with reactive nitrogen species (RNS) are well recognised for playing a dual role as both deleterious and beneficial species. The "two-faced" character of ROS is substantiated by growing body of evidence that ROS within cells act as secondary messengers in intracellular signalling cascades, which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumourigenic species. The cumulative production of ROS/RNS through either endogenous or exogenous insults is termed oxidative stress and is common for many types of cancer cell that are linked with altered redox regulation of cellular signalling pathways. Oxidative stress induces a cellular redox imbalance which has been found to be present in various cancer cells compared with normal cells; the redox imbalance thus may be related to oncogenic stimulation. DNA mutation is a critical step in carcinogenesis and elevated levels of oxidative DNA lesions (8-OH-G) have been noted in various tumours, strongly implicating such damage in the etiology of cancer. It appears that the DNA damage is predominantly linked with the initiation process. This review examines the evidence for involvement of the oxidative stress in the carcinogenesis process. Attention is focused on structural, chemical and biochemical aspects of free radicals, the endogenous and exogenous sources of their generation, the metal (iron, copper, chromium, cobalt, vanadium, cadmium, arsenic, nickel)-mediated formation of free radicals (e.g. Fenton chemistry), the DNA damage (both mitochondrial and nuclear), the damage to lipids and proteins by free radicals, the phenomenon of oxidative stress, cancer and the redox environment of a cell, the mechanisms of carcinogenesis and the role of signalling cascades by ROS; in particular, ROS activation of AP-1 (activator protein) and NF-B (nuclear factor kappa B) signal transduction pathways, which in turn lead to the transcription of genes involved in cell growth regulatory pathways. The role of enzymatic (superoxide dismutase (Cu, Zn-SOD, Mn-SOD), catalase, glutathione peroxidase) and non-enzymatic antioxidants (Vitamin C, Vitamin E, carotenoids, thiol antioxidants (glutathione, thioredoxin and lipoic acid), flavonoids, selenium and others) in the process of carcinogenesis as well as the antioxidant interactions with various regulatory factors, including Ref-1, NF-B, AP-1 are also reviewed.

Plant secondary metabolites are unique sources for pharmaceuticals, food additives, flavors, and other industrial materials. Accumulation of such metabolites often occurs in plants subjected to stresses including various elicitors or signal molecules. Understanding signal transduction paths underlying elicitor-induced production of secondary metabolites is important for optimizing their commercial production. This paper summarizes progress made on several aspects of elicitor signal transduction leading to production of plant secondary metabolites, including: elicitor signal perception by various receptors of plants; avirulence determinants and corresponding plant R proteins; heterotrimeric and small GTP binding proteins; ion fluxes, especially Ca 2+ influx, and Ca 2+ signaling; medium alkalinization and cytoplasmic acidification; oxidative burst and reactive oxygen species; inositol 0734-9750/$ -see front matter D (L.C. Davis)8 [email protected] (R. Verpoorte).

A relatively simple but sensitive and reliable method ofquantitating the oxygen-radical absorbing capacity (ORAC) of antioxidants in serum using a few #l is described. In this assay system, ~-phycoerythrin (~-PE) is used as an indicator protein, 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) as a peroxyl radical generator, and 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox, a water-soluble vitamin E analogue) as a control standard. Results are expressed as ORAC units, where 10RAC unit equals the net protection produced by l ~M Trolox. The uniqueness of this assay is that total antioxidant capacity of a sample is estimated by taking the oxidation reaction to completion. At this point all of the nonprotein antioxidants (which include a-tocopherol, vitamin C, E-carotene, uric acid, and bilirubin) and most of the albumin in the sample are oxidized by the peroxyl radical. Results are quantified by measuring the protection produced by antioxidants. This solves many problems associated with kinetics or lag-time measurements. A linear correlation of ORAC value with concentration of serum, Trolox, vitamin C, uric acid, and bovine albumin is demonstrated. The coefficient of variation within a run is found to be about 2% and from run to run about 5%. Trolox, a-tocopherol, vitamin C,/3-carotene, uric acid, and bilirubin completely protect B-PE from oxidation, while bovine albumin protects/3-PE only partially. On a molar basis, the relative peroxyl radical absorbance capacity of Trolox, a-tocopherol acid succinate, uric acid, bilirubin, and vitamin C is l : 1 : 0.92 : 0.84 : 0.52. Bovine albumin per unit weight has a lower peroxyi absorbing capacity than these antioxidants. However, the serum protein fraction, containing some lipid-soluble antioxidants, represents the major contributor to the ORAC value found in whole serum. The minimum amount of vitamin C and uric acid which could still be detectable when added to a serum supernatant fraction is 1.5/~g and 0.59 #g, respectively, which account for about 1% of the total ORAC value of the serum supernatant fraction.

To describe the importance of the antioxidant enzymes superoxide dismutase, glutathione peroxidase, and catalase working together in human cells against toxic reactive oxygen species, their relationship with several pathophysiologic processes and their possible therapeutic implications. Conclusions: Reactive oxygen species (ROS) are involved in the cell growth, differentiation, progression, and death. Low concentrations of ROS may be beneficial or even indispensable in processes such as intracellular signaling and defense against micro-organisms. Nevertheless, higher amounts of ROS play a role in the aging process as well as in a number of human disease states, including cancer, ischemia, and failures in immunity and endocrine functions. As a safeguard against the accumulation of ROS, several nonenzymatic and enzymatic antioxidant activities exist. Therefore, when oxidative stress arises as a consequence of a pathologic event, a defense system promotes the regulation and expression of these enzymes.

Radiation hazards in outer space present an enormous challenge for the biological safety of astronauts. A deleterious effect of radiation is the production of reactive oxygen species, which result in damage to biomolecules (e.g., lipid, protein, amino acids, and DNA). Understanding free radical biology is necessary for designing an optimal nutritional countermeasure against space radiation–induced cytotoxicity. Free radicals (e.g., superoxide, nitric oxide, and hydroxyl radicals) and other reactive species (e.g., hydrogen peroxide, peroxynitrite, and hypochlorous acid) are produced in the body, primarily as a result of aerobic metabolism. Antioxidants (e.g., glutathione, arginine, citrulline, taurine, creatine, selenium, zinc, vitamin E, vitamin C, vitamin A, and tea polyphenols) and antioxidant enzymes (e.g., superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidases) exert synergistic actions in scavenging free radicals. There has been growing evidence over the past three decades showing that malnutrition (e.g., dietary deficiencies of protein, selenium, and zinc) or excess of certain nutrients (e.g., iron and vitamin C) gives rise to the oxidation of biomolecules and cell injury. A large body of the literature supports the notion that dietary antioxidants are useful radioprotectors and play an important role in preventing many human diseases (e.g., cancer, atherosclerosis, stroke, rheumatoid arthritis, neurodegeneration, and diabetes). The knowledge of enzymatic and non-enzymatic oxidative defense mechanisms will serve as a guiding principle for establishing the most effective nutrition support to ensure the biological safety of manned space missions.

Although the underlying molecular causes of aging are not entirely clear, hormetic agents like exercise, heat, and calorie restriction may generate a mild pro-oxidant stress that induces cell protective responses to promote healthy aging. As an individual ages, many cellular and physiological processes decline, including wound healing and reparative angiogenesis. This is particularly critical in patients with chronic non-healing wounds who tend to be older. We are interested in the potential beneficial effects of hyperbaric oxygen as a mild hormetic stress on human microvascular endothelial cells. We analyzed global gene expression changes in human endothelial cells following a hyperbaric exposure comparable to a clinical treatment. Our analysis revealed an upregulation of antioxidant, cytoprotective, and immediate early genes. This increase coincided with an increased resistance to a lethal oxidative stress. Our data indicate that hyperbaric oxygen can induce protection against oxidative insults in endothelial cells and may provide an easily administered hormetic treatment to help promote healthy aging.

Silver nanoparticles (Ag-np) are being used increasingly in wound dressings, catheters, and various household products due to their antimicrobial activity. The toxicity of starch-coated silver nanoparticles was studied using normal human lung fibroblast cells (IMR-90) and human glioblastoma cells (U251). The toxicity was evaluated using changes in cell morphology, cell viability, metabolic activity, and oxidative stress. Ag-np reduced ATP content of the cell caused damage to mitochondria and increased production of reactive oxygen species (ROS) in a dose-dependent manner. DNA damage, as measured by single cell gel electrophoresis (SCGE) and cytokinesis blocked micronucleus assay (CBMN), was also dose-dependent and more prominent in the cancer cells. The nanoparticle treatment caused cell cycle arrest in G 2 /M phase possibly due to repair of damaged DNA. Annexin-V propidium iodide (PI) staining showed no massive apoptosis or necrosis. The transmission electron microscopic (TEM) analysis indicated the presence of Ag-np inside the mitochondria and nucleus, implicating their direct involvement in the mitochondrial toxicity and DNA damage. A possible mechanism of toxicity is proposed which involves disruption of the mitochondrial respiratory chain by Ag-np leading to production of ROS and interruption of ATP synthesis, which in turn cause DNA damage. It is anticipated that DNA damage is augmented by deposition, followed by interactions of Ag-np to the DNA leading to cell cycle arrest in the G 2 /M phase. The higher sensitivity of U251 cells and their arrest in G 2 /M phase could be explored further for evaluating the potential use of Ag-np in cancer therapy.

Fourteen tropical fruits from south Florida (red guava, white guava, carambola, red pitaya (red dragon), white pitaya (white dragon), mamey sapote, sapodilla, lychee, longan, green mango, ripe mango, green papaya, and ripe papaya) were evaluated for antioxidant activity, total soluble phenolics (TSP), total ascorbic acid (TAA), total dietary fiber (TDF), and pectin. ORAC (oxygen radical absorbance capacity) and DPPH (1,1-diphenyl-2-picrylhydrazyl, radical scavenging activity) assays were used to determine antioxidant activity. The TSP, ORAC, and DPPH ranged from 205.4 to 2316.7 g gallic acid equiv/g puree, <0.1 to 16.7 µmol Trolox equiv/g puree, and 2.1 to 620.2 µg gallic acid equiv/g puree, respectively. The TAA, TDF, and pectin ranged from 7.5 to 188.8 mg/100 g, 0.9 to 7.2 g/100 g, and 0.20 to 1.04 g/100 g, respectively. The antioxidant activities, TSP, TAA, TDF, and pectin were influenced by cultivar (papaya, guava, and dragon fruit) and ripening stage (papaya and/or mango). Antioxidant activity showed high correlations with levels of TSP compounds (r ) 0.96) but low correlations with levels of ascorbic acid (r ) 0.35 and 0.23 for ORAC and DPPH data, respectively). The antioxidant activities evaluated by both ORAC and DPPH showed similar trends where red guava and carambola exhibited the highest and sapodilla and green papaya exhibited the lowest levels. Guava and mamey sapote exhibited the highest TDF and pectin levels. Many of the tropical fruits were shown to contain an abundance of hydrolyzable tannins, ellagic acid conjugates, and flavone glycosides. Preliminary descriptions are given of the phenols in red/white pitaya (dragonfruit), lychee, and mamey sapote, these fruit being thus far uncharacterized in the literature.

Plant secondary metabolites are unique sources for pharmaceuticals, food additives, flavors, and other industrial materials. Accumulation of such metabolites often occurs in plants subjected to stresses including various elicitors or signal molecules. Understanding signal transduction paths underlying elicitor-induced production of secondary metabolites is important for optimizing their commercial production. This paper summarizes progress made on several aspects of elicitor signal transduction leading to production of plant secondary metabolites, including: elicitor signal perception by various receptors of plants; avirulence determinants and corresponding plant R proteins; heterotrimeric and small GTP binding proteins; ion fluxes, especially Ca2+ influx, and Ca2+ signaling; medium alkalinization and cytoplasmic acidification; oxidative burst and reactive oxygen species; inositol trisphosphates and cyclic nucleotides (cAMP and cGMP); salicylic acid and nitric oxide; jasmonate, ethylene, and abscisic acid signaling; oxylipin signals such as allene oxide synthase-dependent jasmonate and hydroperoxide lyase-dependent C12 and C6 volatiles; as well as other lipid messengers such as lysophosphatidylcholine, phosphatidic acid, and diacylglycerol. All these signal components are employed directly or indirectly by elicitors for induction of plant secondary metabolite accumulation. Cross-talk between different signaling pathways is very common in plant defense response, thus the cross-talk amongst these signaling pathways, such as elicitor and jasmonate, jasmonate and ethylene, and each of these with reactive oxygen species, is discussed separately. This review also highlights the integration of multiple signaling pathways into or by transcription factors, as well as the linkage of the above signal components in elicitor signaling network through protein phosphorylation and dephosphorylation. Some perspectives on elicitor signal transduction and plant secondary metabolism at the transcriptome and metabolome levels are also presented.

Oxidative stress is linked with many pathologies ranging from cancer to neurodegenerative disorders and antioxidants have presumably therapeutic value in such diseases. In this review, we categorize different direct and indirect mechanisms by which antioxidants exert their action. These include scavenging and metal chelating effects, mimicking the antioxidant enzymes or upregulation of their expression, activation of nuclear factor erythroid 2-related factor 2 (Nrf2), increasing the activity of sirtuins and inhibition of pro-oxidant enzymes among others. Recent findings on the most frequently investigated antioxidants including polyphenolics, thiolics, spin trapping agents, SOD mimetics, inducers of heme oxygenase-1 and nitric oxide synthase, activators of Nrf2, NADPH oxidase inhibitors and herbal supplements are summarized. Furthermore, the antioxidant effects of drugs that are clinically used for other pharmacological purposes including ACE inhibitors and statins are discussed. Cost-effectiveness and adverse effects of antioxidants are also evaluated. Since antioxidant therapy has failed in many instances, we have classified the reasons that may explain these shortcomings in different categories. Novel approaches to antioxidant therapy, that include mitochondria-targeting drugs, antioxidant gene therapy and approaches for improvement of cell uptake and alteration of subcellular compartment localization are also described. In the end, "shadows" that are shortcomings of antioxidant therapy as well as "lights" that include positive outcomes are addressed. It is concluded that if we learn from failures, invest on agents with higher potential and take advantage of novel emerging approaches, antioxidants could be an asset for the management of certain carefully chosen oxidative stress-related diseases. vii. pulmonary diseases, including chronic obstructive pulmonary disease (COPD) [22] and asthma [23]; viii. chronic kidney disease (CKD) [24]; ix. psychiatric disorders, including depression [25], bipolar disorder [26] and schizophrenia [27].

Wireless technologies are ubiquitous today and the mobile phones are one of the prodigious output of this technology. Although the familiarization and dependency of mobile phones is growing at an alarming pace, the biological effects due to the exposure of radiations have become a subject of intense debate. The present evidence on mobile phone radiation exposure is based on scientific research and public policy initiative to give an overview of what is known of biological effects that occur at radiofrequency (RF)/ electromagnetic fields (EMFs) exposure. The conflict in conclusions is mainly because of difficulty in controlling the affecting parameters. Biological effects are dependent not only on the distance and size of the object (with respect to the object) but also on the environmental parameters. Health endpoints reported to be associated with RF include childhood leukemia, brain tumors, genotoxic effects, neurological effects and neurodegenerative diseases, immune system dereg...

Key Words programmed cell death, abiotic stress, pathogen defense s Abstract Several reactive oxygen species (ROS) are continuously produced in plants as byproducts of aerobic metabolism. Depending on the nature of the ROS species, some are highly toxic and rapidly detoxified by various cellular enzymatic and nonenzymatic mechanisms. Whereas plants are surfeited with mechanisms to combat increased ROS levels during abiotic stress conditions, in other circumstances plants appear to purposefully generate ROS as signaling molecules to control various processes including pathogen defense, programmed cell death, and stomatal behavior. This review describes the mechanisms of ROS generation and removal in plants during development and under biotic and abiotic stress conditions. New insights into the complexity and roles that ROS play in plants have come from genetic analyses of ROS detoxifying and signaling mutants. Considering recent ROS-induced genomewide expression analyses, the possible functions and mechanisms for ROS sensing and signaling in plants are compared with those in animals and yeast.

Aims & Scope This clinically orientated journal is an important platform from which to present information generated within the international fi eld of biological psychiatry. The World Journal of Biological Psychiatry aims to increase knowledge of clinical and basic research and covers a broad spectrum of diverse categories. Its readership includes clinical psychiatrists, educators, scientists and students interested in learning more about the latest developments .

As a result of the industrial revolution, anthropogenic activities have enhanced there distribution of many toxic heavy metals from the earth&#39;s crust to different environmental compartments. Environmental pollution by toxic heavy metals is increasing worldwide, and poses a rising threat to both the environment and to human health.Plants are exposed to heavy metals from various sources: mining and refining of ores, fertilizer and pesticide applications, battery chemicals, disposal of solid wastes(including sewage sludge), irrigation with wastewater, vehicular exhaust emissions and adjacent industrial activity.Heavy metals induce various morphological, physiological, and biochemical dysfunctions in plants, either directly or indirectly, and cause various damaging effects. The most frequently documented and earliest consequence of heavy metal toxicity in plants cells is the overproduction of ROS. Unlike redox-active metals such as iron and copper, heavy metals (e.g, Pb, Cd, Ni, AI,...

Oxidative stress generated by an imbalance between reactive oxygen species (ROS) and antioxidants contributes to the pathogenesis of arthritis, cancer, cardiovascular, liver and respiratory diseases. Proinflammatory cytokines and growth factors stimulate ROS production as signaling mediators. Antioxidants such as N-acetylcysteine (NAC) have been used as tools for investigating the role of ROS in numerous biological and pathological processes. NAC inhibits activation of c-Jun N-terminal kinase, p38 MAP kinase and redox-sensitive activating protein-1 and nuclear factor kappa B transcription factor activities regulating expression of numerous genes. NAC can also prevent apoptosis and promote cell survival by activating extracellular signal-regulated kinase pathway, a concept useful for treating certain degenerative diseases. NAC directly modifies the activity of several proteins by its reducing activity. Despite its nonspecificity, ability to modify DNA and multiple molecular modes of action, NAC has therapeutic value for reducing endothelial dysfunction, inflammation, fibrosis, invasion, cartilage erosion, acetaminophen detoxification and transplant prolongation.

Copper (Cu), a redox active metal, is an essential nutrient for all species studied to date. During the past decade, there has been increasing interest in the concept that marginal deficits of this element can contribute to the development and progression of a number of disease states including cardiovascular disease and diabetes. Deficits of this nutrient during pregnancy can result in gross structural malformations in the conceptus, and persistent neurological and immunological abnormalities in the offspring. Excessive amounts of Cu in the body can also pose a risk. Acute Cu toxicity can result in a number of pathologies, and in severe cases, death. Chronic Cu toxicity can result in liver disease and severe neurological defects. The concept that elevated ceruloplasmin is a risk factor for certain diseases is discussed. In this paper, we will review recent literature on the potential causes of Cu deficiency and Cu toxicity, and the pathological consequences associated with the above. Finally, we will review some of the potential biochemical lesions that might underlie these pathologies. Given that oxidative stress is a characteristic of Cu deficiency, the role of Cu in the oxidative defense system will receive special attention. The concept that excess Cu may be a precipitating factor in Alzhei-merÕs disease is discussed.

Ageing results from complex genetically and epigenetically programmed processes that are elicited in part by noxious or stressful events that cause programmed cell death. Here, we report that administration of spermidine, a natural polyamine whose intracellular concentration declines during human ageing, markedly extended the lifespan of yeast, flies and worms, and human immune cells. In addition, spermidine administration potently inhibited oxidative stress in ageing mice. In ageing yeast, spermidine treatment triggered epigenetic deacetylation of histone H3 through inhibition of histone acetyltransferases (HAT), suppressing oxidative stress and necrosis. Conversely, depletion of endogenous polyamines led to hyperacetylation, generation of reactive oxygen species, early necrotic death and decreased lifespan. The altered acetylation status of the chromatin led to significant upregulation of various autophagy-related transcripts, triggering autophagy in yeast, flies, worms and human cells. Finally, we found that enhanced autophagy is crucial for polyamine-induced suppression of necrosis and enhanced longevity.

Reactive oxygen species (ROS) are constantly generated and eliminated in the biological system, and play important roles in a variety of normal biochemical functions and abnormal pathological processes. Growing evidence suggests that cancer cells exhibit increased intrinsic ROS stress, due in part to oncogenic stimulation, increased metabolic activity, and mitochondrial malfunction. Since the mitochondrial respiratory chain (electron transport complexes) is a major source of ROS generation in the cells, the vulnerability of the mitochondrial DNA to ROS-mediated damage appears to be a mechanism to amplify ROS stress in cancer cells. The escalated ROS generation in cancer cells serves as an endogenous source of DNA-damaging agents that promote genetic instability and development of drug resistance. Malfunction of mitochondria also alters cellular apoptotic response to anticancer agents. Despite the negative impacts of increased ROS in cancer cells, it is possible to exploit this biochemical feature and develop novel therapeutic strategies to preferentially kill cancer cells through ROS-mediated mechanisms. This article reviews ROS stress in cancer cells, its underlying mechanisms and relationship with mitochondrial malfunction and alteration in drug sensitivity, and suggests new therapeutic strategies that take advantage of increased ROS in cancer cells to enhance therapeutic activity and selectivity.

Lipid peroxidation is a primary cause of quality deterioration in meat and meat products. Free radical chain reaction is the mechanism of lipid peroxidation and reactive oxygen species (ROS) such as hydroxyl radical and hydroperoxyl radical are the major initiators of the chain reaction. Lipid peroxyl radical and alkoxyl radical formed from the initial reactions are also capable of abstracting a hydrogen atom from lipid molecules to initiate the chain reaction and propagating the chain reaction. Much attention has been paid to the role of iron as a primary catalyst of lipid peroxidation. Especially, heme proteins such as myoglobin and hemoglobin and "free" iron have been regarded as major catalysts for initiation, and iron-oxygen complexes (ferryl and perferryl radical) are even considered as initiators of lipid peroxidation in meat and meat products. Yet, which iron type and how iron is involved in lipid peroxidation in meat are still debatable. This review is focused on the potential roles of ROS and iron as primary initiators and a major catalyst, respectively, on the development of lipid peroxidation in meat and meat products. Effects of various other factors such as meat species, muscle type, fat content, oxygen availability, cooking, storage temperature, the presence of salt that affect lipid peroxidation in meat and meat products are also discussed.

Regardless of the reality that the deactivation of bacteria by different electrochemical (EC) disinfection means has been largely reported in the literature, the influence of process variables and reactor conception on kill performance has not been well comprehended. Moreover, a small number of researches focused on the mechanisms of EC disinfection. This review concentrates on EC microbial killing mechanisms. Several related and pertinent references are examined and key mechanisms are revealed. Some mechanisms have been suggested to interpret the deadliness of EC application, comprising (1) oxidative stress and cell loss of life because of electrochemically produced oxidants, (2) irreversible permeabilization of cell membranes by the placed electric field (EF), (3) EC oxidation of vital cellular constituents during exposure to electric current or induced EFs, and (4) electrosorption of negatively charged microorganisms cells to the anode surface followed by direct electron transfer reaction.

During the past two decades, coral reefs have experienced extensive degradation worldwide. One etiology for this global degradation is a syndrome known as coral bleaching. Mass coral bleaching events are correlated with increased sea-surface temperatures, however, the cellular mechanism underlying this phenomenon is uncertain. To determine if oxidative stress plays a mechanistic role in the process of sea-surface temperature-related coral bleaching, we examined corals along a depth transect in the Florida Keys over a single season that was characterized by unusually high sea-surface temperatures. We observed strong positive correlations between accumulation of oxidative damage products and bleaching in corals over a year of sampling. High levels of antioxidant enzymes and small heat-shock proteins were negatively correlated with levels of oxidative damage products. Corals that experienced oxidative stress had higher chaperonin levels and protein turnover activity. Our results indicate that coral bleaching is tightly coupled to the antioxidant and cellular stress capacity of the symbiotic coral, supporting the mechanistic model that coral bleaching (zooxanthellae loss) may be a final strategy to defend corals from oxidative stress.

Arbuscular mycorrhizal fungi (AMF) have repeatedly been demonstrated to alleviate heavy metal stress of plants. The current manuscript summarizes results obtained to date on the colonization of plants by AMF in heavy metal soils, the depositions of heavy metals in plant and fungal structures and the potential to use AMF-plant combinations in phytoremediation, with emphasis on pennycresses (Thlaspi ssp.). The focus of this manuscript is to describe and discuss studies on the expression of genes in plants and fungi under heavy metal stress. The summary is followed by data on differential gene expression in extraradical mycelia (ERM) of in vitro cultured Glomus intraradices Sy167 supplemented with different heavy metals (Cd, Cu or Zn). The expression of several genes encoding proteins potentially involved in heavy metal tolerance varied in their response to different heavy metals. Such proteins included a Zn transporter, a metallothionein, a 90 kD heat shock protein and a glutathione S-transferase (all assignments of protein function are putative). Studies on the expression of the selected genes were also performed with roots of Medicago truncatula grown in either a natural, Zn-rich heavy metal ''Breinigerberg'' soil or in a non-polluted soil supplemented with 100 lM ZnSO 4 . The transcript levels of the genes analyzed were enhanced up to eight fold in roots grown in the heavy metal-containing soils. The data obtained demonstrate the heavy metal-dependent expression of different AMF genes in the intra-and extraradical mycelium. The distinct induction of genes coding for proteins possibly involved in the alleviation of damage caused by reactive oxygen species (a 90 kD heat shock protein and a glutathione S-transferase) might indicate that heavy metal-derived oxidative stress is the primary concern of the fungal partner in the symbiosis.

Pharmacotherapy using natural substances can be currently regarded as a very promising future alternative to conventional therapy. With the rapid development of biotechnologies and analytical techniques, a great number of methods have been developed for the identification and quantification of the material, extracts, and products of natural ingredients. The advances available today. The need for safer drugs without side effects has led to the use of natural ingredients with proven safety. In recent years, some bioactive polysaccharides isolated from natural sources have attracted much attention in the field of biochemistry and pharmacology. As an example, polysaccharides or their glycoconjugates were shown to exhibit multiple biological activities including anticarcinogenic, anticoagulant, immunostimulating, antioxidant, etc. During the last several years, we have witnessed a steady expansion in the number of publications that focus in antioxidant polysaccharides. This review presents current findings on the latest advancements and trends in antioxidant polysaccharides isolated from the following: plants, fungi, bacteria, animal sources, and algae. Some interesting studies focus on investigation of the relationship between their structure and antioxidant activity, elucidation of their antioxidant mechanism at the molecular level, and improvement of their various biological activities by chemical modifications. Although the mechanism of their antioxidant action is still not completely clear, these polysaccharides are suggested to enhance cell-mediated immune responses in vivo and in vitro and act as biological response modifiers.

The mitochondrion is the most important organelle in determining continued cell survival and cell death. Mitochondrial dysfunction leads to many human maladies, including cardiovascular diseases, neurodegenerative disease, and cancer. These mitochondria-related pathologies range from early infancy to senescence. The central premise of this review is that if mitochondrial abnormalities contribute to the pathological state, alleviating the mitochondrial dysfunction would contribute to attenuating the severity or progression of the disease. Therefore, this review will examine the role of mitochondria in the etiology and progression of several diseases and explore potential therapeutic benefits of targeting mitochondria in mitigating the disease processes. Indeed, recent advances in mitochondrial biology have led to selective targeting of drugs designed to modulate and manipulate mitochondrial function and genomics for therapeutic benefit. These approaches to treat mitochondrial dysfunction rationally could lead to selective protection of cells in different tissues and various disease states. However, most of these approaches are in their infancy. Antioxid. Redox Signal. 13, 279-347.

During normal cellular activities, various processes inside of cells produce reactive oxygen species (ROS). Some of the most common ROS are hydrogen peroxide (H 2 O 2 ), superoxide ion (O 2 À ), and hydroxide radical (OH À ). These compounds, when present in a high enough concentration, can damage cellular proteins and lipids or form DNA adducts that may promote carcinogenic activity. The purpose of antioxidants in a physiological setting is to prevent ROS concentrations from reaching a high-enough level within a cell that damage may occur. Cellular antioxidants may be enzymatic (catalase, glutathione peroxidase, superoxide dismutase) or nonenzymatic (glutathione, thiols, some vitamins and metals, or phytochemicals such as isoflavones, polyphenols, and flavanoids).

Reactive oxygen species (ROS) play a multitude of signaling roles in different organisms from bacteria to mammalian cells. They were initially thought to be toxic byproducts of aerobic metabolism, but have now been acknowledged as central players in the complex signaling network of cells. In this review, we will attempt to address several key questions related to the use of ROS as signaling molecules in cells, including the dynamics and specificity of ROS signaling, networking of ROS with other signaling pathways, ROS signaling within and across different cells, ROS waves and the evolution of the ROS gene network.

Myoglobin is a cytoplasmic hemoprotein that is restricted to cardiomyocytes and oxidative skeletal muscle fibers. Myoglobin is a well-characterized protein and numerous studies have established that it has an essential role in facilitated oxygen transport in striated muscles. Recent strategies, using gene disruption technologies, have produced mice that lack myoglobin. These myoglobin deficient mice have a binary phenotype and a subpopulation of these mutant mice is viable and fertile. Characterization of the viable myoglobin null mice has uncovered a number of molecular and cellular adaptive mechanisms that function to promote oxygen delivery in the mutant striated muscle cell. Moreover, cellular and physiological studies, using the myoglobin deficient mouse model, support the conclusion that the functions of myoglobin include: facilitated oxygen transport, the storage of oxygen and a scavenger of nitric oxide or reactive oxygen species. Collectively, the use of genetic mouse model...

Lactic acid bacteria (LAB) constitute a heterogeneous group of bacteria that are traditionally used to produce fermented foods. The industrialization of food bio-transformations increased the economical importance of LAB, as they play a crucial role in the development of the organoleptique and hygienic quality of fermented products. Therefore, the reliability of starter strains in terms of quality and functional properties (important for the development of aroma and texture), but also in terms of growth performance and robustness has become essential. These strains should resist to adverse conditions encountered in industrial processes, for example during starter handling and storage (freeze-drying, freezing or spray-drying). The development of new applications such as life vaccines and probiotic foods reinforces the need for robust LAB since they may have to survive in the digestive tract, resist the intestinal flora, maybe colonize the digestive or uro-genital mucosa and express s...

Ageing is accompanied by the accumulation of damaged molecules in cells due to the injury produced by external and internal stressors. Among them, reactive oxygen species produced by cell metabolism, inflammation or other enzymatic processes are considered key factors. However, later research has demonstrated that a general mitochondrial dysfunction affecting electron transport chain activity, mitochondrial biogenesis and turnover, apoptosis, etc., seems to be in a central position to explain ageing. This key role is based on several effects from mitochondrial-derived ROS production to the essential maintenance of balanced metabolic activities in old organisms. Several studies have demonstrated caloric restriction, exercise or bioactive compounds mainly found in plants, are able to affect the activity and turnover of mitochondria by increasing biogenesis and mitophagy, especially in postmitotic tissues. Then, it seems that mitochondria are in the centre of metabolic procedures to be modified to lengthen lifeor health-span. In this review we show the importance of mitochondria to explain the ageing process in different models or organisms (e.g. yeast, worm, fruitfly and mice). We discuss if the cause of aging is dependent on mitochondrial dysfunction of if the mitochondrial changes observed with age are a consequence of events taking place outside the mitochondrial compartment.

The ongoing West African Ebola epidemic highlights a recurring trend in the zoonotic emergence of virulent pathogens likely to come from bat reservoirs that has caused epidemiologists to ask ‘Are bats special reser- voirs for emerging zoonotic pathogens?’ We collate evidence from the past decade to delineate mitochon- drial mechanisms of bat physiology that have evolved to mitigate oxidative stress incurred during metabolically costly activities such as flight. We further describe how such mechanisms might have generated pleiotropic effects responsible for tumor mitigation and pathogen control in bat hosts. These synergisms may enable ‘spe- cial’ tolerance of intracellular pathogens in bat hosts; paradoxically, this may leave them more susceptible to immunopathological morbidity when attempting to clear extracellular infections such as ‘white-nose syndrome’ (WNS).

Mitochondria are the organelles producing most of the energy and play important roles in a variety of biochemical functions in human cells. Mitochondrial defects can cause ATP deficiency and overproduction of reactive oxygen species, which are the major hallmarks of mitochondrial diseases. Abundant evidence has suggested that mitochondrial dysfunction-elicited oxidative stress can play an important role in the pathogenesis and progression of mitochondrial diseases. Mitochondria can respond to energy deficiency by the retrograde signaling to trigger a number of molecular events to help the human cells to cope with physiological or environmental changes. In this article, we first describe oxidative stress-induced cellular responses including metabolic adaptation, compensatory increase of mitochondrial biogenesis, upregulation of antioxidant enzymes, and alteration of protein acetylation in human cells with mitochondrial dysfunction. In this regard, we review recent findings to elucidate the mechanisms by which human cells motivate their mitochondria and the antioxidant defense system to respond to energy deficiency and oxidative stress, which contribute to the adaptive metabolic reprogramming in mitochondrial diseases. In addition, we emphasize the critical role of the activation of AMPK, Sirt1 and Sirt3 in the metabolic adaptation of human cells harboring mitochondrial DNA mutations. Recent studies have revealed that AMPK and sirtuins-mediated signaling pathways are involved in metabolic reprogramming, which is effected by upregulation of antioxidant defense system and mitochondrial protein acetylation, in human cells with mitochondrial dysfunction. Finally, we discuss several potential modulators of bioenergetic function such as coenzyme Q10, mitochondria-targeting antioxidants, resveratrol, and L-carnitine based on recent findings from studies on human cells and animal models of mitochondrial diseases. Elucidation of the signaling pathway of this adaptive response to oxidative stress triggered by mitochondrial dysfunction may enable us to gain a deeper insight into the communication between mitochondria and the nucleus and guide us to develop novel therapeutic agents for effective treatment of mitochondrial diseases.

The effects of long-term dietary administration of corticosterone (CORT) on the induction of oxidative injury in broiler chickens (Gallus gallus domesticus) were evaluated. The experimental broiler chickens were fed with a diet supplemented with 30 mg CORT/kg diet for 2 weeks from 14 days of age onwards, while control chickens continued to consume the control diet. The growth performance parameters were recorded weekly, and a blood sample was obtained from eight birds of both groups before CORT administration and at 3, 7 and 14 days after treatment. The results showed that chronic CORT administration resulted in enhanced proteolysis and gluconeogenesis. Furthermore, CORT administration may initially induce the formation of reactive oxygen species (ROS) as indirectly reflected by an increase in lipid peroxidation. However, the significantly increased plasma uric acid (UA) and ceruloplasmin (CP) levels after 3 days of treatment indicates an enhancement of the nonenzymatic antioxidant capacity during stress, and in this way, the development of a more severe oxidative injury is alleviated. Broiler chickens seem to adapt to high circulating CORT levels in terms of their redox homeostasis after 3 days of treatment under the present experimental conditions. D

The vast industrial use of nickel has led to environmental pollution by the metal and its by-products during production, recycling, and disposal. Nickel is a known hematotoxic, immunotoxic, hepatotoxic, pulmotoxic, and nephrotoxic agent. Allergic skin reactions are common in individuals who are sensitive to nickel. This article presents a selective review on nickel and its effect on certain metabolically active peripheral tissues of human and animals. The subtopics include nickel sources and uses, exposure pathways, transport, excretion, general health effects, and specific acute and chronic nickel toxicities in peripheral tissues like liver, lungs, and kidneys. The review particularly addresses the nickel-induced generation of reactive oxygen species and increased lipid peroxidation in various metabolically active tissues in humans and animals, and the possible role of vitamin c as a protective antioxidant.

The use of nanoscaled zero-valent iron particles (nZVI) to remediate contaminated soil and groundwater has received increasing amounts of attention within the last decade, primarily due to its potential for broader application, higher reactivity, and cost-effectiveness compared to conventional zero-valent iron applications and other in situ methods. However, the potential environmental risks of nZVI in in situ field scale applications are largely unknown at the present and traditional environmental risk assessment approaches are not yet able to be completed. Therefore, it may not yet be fully clear how to consider the environmental benefits and risks of nZVI for in situ applications. This analysis therefore addresses the challenges of comprehensively considering and weighing the expected environmental benefits and potential risks of this emerging environmentally-beneficial nanotechnology, particularly relevant for environmental engineers, scientists, and decision makers. We find that most of the benefits of using nZVI are based on near-term considerations, and large data gaps currently exist within almost all aspects of environmental exposure and effect assessments. We also find that while a wide range of decision support tools and frameworks alternative to risk assessment are currently available, a thorough evaluation of these should be undertaken in the near future to assess their full relevancy for nZVI at specific sites. Due to the absence of data in environmental risk evaluations, we apply a 'best' and 'worst' case scenario evaluation as a first step to qualitatively evaluate the current state-ofknowledge regarding the potential environmental risks of nZVI. The result of this preliminary qualitative evaluation indicates that at present, there are no significant grounds on which to form the basis that nZVI currently poses a significant, apparent risk to the environment, although the majority of the most serious criteria (i.e. potential for persistency, bioaccumulation, toxicity) are generally unknown. We recommend that in cases where nZVI may be chosen as the 'best' treatment option, short and long-term environmental monitoring is actively employed at these sites. We furthermore recommend the continued development of responsible nZVI innovation and better facilitated information exchange between nZVI developers, nano-risk researchers, remediation industry, and decision makers. (K.D. Grieger), [email protected] (A. Fjordbøge), [email protected] (N.B. Hartmann), [email protected] (E. Eriksson), [email protected] (P.L. Bjerg), [email protected] (A. Baun).

The generation of Reactive Oxygen Species (ROS), H2O2 and OH, has been observed from sulfide mineral containing particles in acidic solutions. The implications of this phenomenon, as a potential microbial stress-causing effect, have been studied previously with respect to thermophilic bioleaching performance in the presence of finely milled pyrite and chalcopyrite concentrates. In this study, the effect of sulfide mineralogy on ROS generation in the absence of microbes under physicochemical conditions typical for the bioleach environment was investigated. The mineralogical and elemental composition of eleven different samples containing sulfide mineral was obtained. These Au, Cu and other base metal-containing sulfide mineral concentrates as well as a milled whole ore of low Cu grade were tested for ROS generation. The whole ore sample and two refractory Au concentrates containing approximately 50% pyrite, generated significantly less ROS compared to the base metal-containing concentrates when compared on a constant surface area loading basis. Sulfide mineral-related variables were correlated with ROS generation. A significant difference was observed between FeS2 and CuFeS2 grades separately, whereas a combined measure of both minerals present in samples showed a consistently strong correlation to ROS generation. The Cu grade, total Cu-containing sulfides and the chalcopyrite content of Cu-containing samples correlated well with ROS generation. However, a common deterministic variable with a strong association to increased ROS generation was not found. A sub-set of samples were subjected to QEMSCAN® for textural analysis. Results suggested that a decrease in sulfide mineral liberation, caused by gangue silicate mineral occlusion to solution, resulted in decreased reactivity as shown in one of the Au-containing samples. Well-liberated chalcopyrite and pyrite phases corresponded to increased reactivity of samples. Pyrite, which was present in all of the reactive samples, was shown to be associated with other sulfide minerals, implicating its importance in galvanic interactions. Micro-analysis of chalcopyrite and pyrite phases from highly reactive samples showed an abundance of particles with extensive cracking and the possible presence of secondary transformation phases (szomolnokite). These results suggest that sulfide mineralogy, liberation and extent of physical processing affect sulfide mineral concentrate reactivity in acidic solutions.► Metal-containing sulfide mineral concentrates generate ROS (H2O2 + OH). ► ROS generation linked to decreased thermophilic bioleaching performance. ► ROS generation consistently correlated to combined Py + Cp content. ► Sulfide liberation and association effects ROS generation under acidic conditions. ► Increased “micro-cracked” particle volume results in increased sample reactivity.

Beta-glucans participate in the processes of repair, metabolism and detoxification, and affect the overall health of the body counteract the pathological conditions of reactive oxygen and nitrogen and the processes in which they participate. Reactive oxygen species (ROS) and nitrogen (RNS) play an important role in the pathogenesis of many diseases. Production of ROS is an integral part of aerobic metabolism of cells. Physiological concentrations of ROS play an important role in proper functioning of many cellular processes, and their overproduction occurs during induced oxidative stress. Very closely associated with oxidative stress is nitrosative stress. Nitric oxide (NO) reacts with molecular oxygen, superoxide anion radical and metal cations to give more reactive oxygen species. Reactive oxygen and nitrogen react with proteins to cause impairment of their function by oxidation or nitrosylation of amino acid residues, which can direct the path of apoptotic cells. In addition, nit...

Silver nanoparticles (Ag-np) are being used increasingly in wound dressings, catheters, and various household products due to their antimicrobial activity. The toxicity of starch-coated silver nanoparticles was studied using normal human lung fibroblast cells (IMR-90) and human glioblastoma cells (U251). The toxicity was evaluated using changes in cell morphology, cell viability, metabolic activity, and oxidative stress. Ag-np reduced ATP content of the cell caused damage to mitochondria and increased production of reactive oxygen species (ROS) in a dose-dependent manner. DNA damage, as measured by single cell gel electrophoresis (SCGE) and cytokinesis blocked micronucleus assay (CBMN), was also dose-dependent and more prominent in the cancer cells. The nanoparticle treatment caused cell cycle arrest in G 2 /M phase possibly due to repair of damaged DNA. Annexin-V propidium iodide (PI) staining showed no massive apoptosis or necrosis. The transmission electron microscopic (TEM) analysis indicated the presence of Ag-np inside the mitochondria and nucleus, implicating their direct involvement in the mitochondrial toxicity and DNA damage. A possible mechanism of toxicity is proposed which involves disruption of the mitochondrial respiratory chain by Ag-np leading to production of ROS and interruption of ATP synthesis, which in turn cause DNA damage. It is anticipated that DNA damage is augmented by deposition, followed by interactions of Ag-np to the DNA leading to cell cycle arrest in the G 2 /M phase. The higher sensitivity of U251 cells and their arrest in G 2 /M phase could be explored further for evaluating the potential use of Ag-np in cancer therapy.

Your article is protected by copyright and all rights are held exclusively by Springer-Verlag Berlin Heidelberg. This e-offprint is for personal use only and shall not be selfarchived in electronic repositories. If you wish to self-archive your article, please use the accepted manuscript version for posting on your own website. You may further deposit the accepted manuscript version in any repository, provided it is only made publicly available 12 months after official publication or later and provided acknowledgement is given to the original source of publication and a link is inserted to the published article on Springer's website. The link must be accompanied by the following text: "The final publication is available at link.springer.com".