Reactive Oxygen And Nitrogen Species Levels Research Articles

Effect of acute cadmium exposure on oxidative stress and antioxidant system of the scallop Aequipecten tehuelchus

This study aimed to assess the impact of acute exposure (96 h) to Cd in gills, digestive gland and muscle of the Tehuelche scallop Aequipecten tehuelchus from San José gulf in Patagonia, Argentina. Scallops were exposed to Cd concentrations of 0, 25, 50, 100, 150, 204, 275, 371, and 500 μg/L, and mortality rates were recorded after 96 h of exposure. Surviving organisms were analyzed for the biochemical response through reactive oxygen and nitrogen species (RONS), activities of catalase (CAT) and glutathione-S-transferase (GST), metallothioneins (MT), lipid peroxidation (LPO) and liposoluble antioxidants α-tocopherol (α-T) and β-carotene (β-C). The mean lethal concentration (LC50) was 155.8 μg Cd/L, a lower value than other scallops' species, showing that A. tehuelchus has a particular sensitivity to Cd. In the three tissues, at all exposure concentrations, there was no significant response in RONS levels, GST activity or LPO. Nevertheless, CAT activity and α-T levels decreased in the gills but increased in the digestive gland, with no significant response in the muscle. Two-way ANOVA revealed a significant interaction between Cd concentration and tissue on MT, which increased significantly in gills, decreased in digestive gland with 100 compared to 50 μg Cd/L; whereas in muscle a significant increase was observed with 25 μg Cd/L compared to control. The results show a significant effect of Cd in scallop's gills on CAT activity and α-T levels, highlighting this tissue as the primary target against relevant concentrations of metal in seawater. The effect on digestive gland and muscle was minimal. The overall results suggest that Cd toxicity is tissue-specific. This study will help reduce the existence knowledge gap regarding potential impacts of acute exposure to Cd in a bivalve species with high ecological and commercial importance, as well as identifying the most responsive biomarkers associated with Cd stress for monitoring assessment.

Oxidative modification in nuclear and mitochondrial DNA and its removal in A549 human lung cancer cells exposed to cold atmospheric-pressure plasma

Non-thermal atmospheric-pressure plasma has emerged as a useful tool in life science research and medicine. Plasma irradiation generates reactive oxygen and nitrogen species (RONS) that stimulate various cellular responses. In this study, we investigated oxidative damage to nuclear and mitochondrial DNA in A549 human lung cancer cells exposed to a helium atmospheric-pressure plasma jet (APPJ). APPJ irradiation decreased the viability of A549 cells and increased intracellular RONS levels. The formation of 8-oxoguanine (8-oxoG), a representative oxidized form of a DNA base, was observed in nuclear DNA. Pretreatment of A549 cells with an antioxidant reagent prior to APPJ irradiation suppressed the increase in 8-oxoG level. The 8-oxoG level gradually decreased during cell culture, suggesting that 8-oxoG was removed from nuclear DNA after APPJ irradiation. Formation of 8-oxoG was also observed in mitochondrial DNA, indicating the accumulation of RONS in mitochondria.

Injectable reactive oxygen and nitrogen species-controlling hydrogels for tissue regeneration: current status and future perspectives.

The dual role of reactive oxygen and nitrogen species (RONS) in physiological and pathological processes in biological systems has been widely reported. It has been recently suggested that the regulation of RONS levels under physiological and pathological conditions is a potential therapy to promote health and treat diseases, respectively. Injectable hydrogels have been emerging as promising biomaterials for RONS-related biomedical applications owing to their excellent biocompatibility, three-dimensional and extracellular matrix-mimicking structures, tunable properties and easy functionalization. These hydrogels have been developed as advanced injectable platforms for locally generating or scavenging RONS, depending on the specific conditions of the target disease. In this review article, the design principles and mechanism by which RONS are generated/scavenged from hydrogels are outlined alongside a discussion of their in vitro and in vivo evaluations. Additionally, we highlight the advantages and recent developments of these injectable RONS-controlling hydrogels for regenerative medicines and tissue engineering applications.

Oxidative stress in obesity and insulin resistance

Since obesity is one of the main factors in the development of insulin resistance (IR) and is also associated with increased oxidative stress (OxS) rate, this study aims to review the published literature to collate and provide a comprehensive summary of the studies related to the status of the OxS in the pathogenesis of obesity and related IR. OxS represents an imbalance between the production of reactive oxygen and nitrogen species (RONS) and the capacity of the antioxidant defense system (AOS) to neutralize RONS. A steady-state of RONS level is maintained through endogenous enzymatic and non-enzymatic AOS components. Three crucial enzymes, which suppress the formation of free radicals, are superoxide dismutases, catalases, and glutathione peroxidases. The second line of AOS includes non-enzymatic components such as vitamins C and E, coenzyme Q, and glutathione which neutralizes free radicals by donating electrons to RONS. Emerging evidence suggests that high RONS levels contribute to the progression of OxS in obesity by activating inflammatory pathways and thus leading to the development of pathological states, including IR. In addition, decreased level of AOS components in obesity increases the susceptibility to oxidative tissue damage and further progression of its comorbidities. Increased OxS in accumulated adipose tissue should be an imperative target for developing new therapies in obesity-related IR.

Role of RONS and eIFs in Cancer Progression.

Various research works have piled up conflicting evidence questioning the effect of oxidative stress in cancer. Reactive oxygen and nitrogen species (RONS) are the reactive radicals and nonradical derivatives of oxygen and nitrogen. RONS can act as a double-edged weapon. On the one hand, RONS can promote cancer initiation through activating certain signal transduction pathways that direct proliferation, survival, and stress resistance. On the other hand, they can mitigate cancer progression via their resultant oxidative stress that causes many cancer cells to die, as some recent studies have proposed that high RONS levels can limit the survival of cancer cells during certain phases of cancer development. Similarly, eukaryotic translation initiation factors are key players in the process of cellular transformation and tumorigenesis. Dysregulation of such translation initiation factors in the form of overexpression, downregulation, or phosphorylation is associated with cancer cell's altering capability of survival, metastasis, and angiogenesis. Nonetheless, eIFs can affect tumor age-related features. Data shows that alternating the eukaryotic translation initiation apparatus can impact many downstream cellular signaling pathways that directly affect cancer development. Hence, researchers have been conducting various experiments towards a new trajectory to find novel therapeutic molecular targets to improve the efficacy of anticancer drugs as well as reduce their side effects, with a special focus on oxidative stress and initiation of translation to harness their effect in cancer development. An increasing body of scientific evidence recently links oxidative stress and translation initiation factors to cancer-related signaling pathways. Therefore, in this review, we present and summarize the recent findings in this field linking certain signaling pathways related to tumorigeneses such as MAPK and PI3K, with either RONS or eIFs.

Cytoprotective effects of antioxidant supplementation on mesenchymal stem cell therapy

Mesenchymal stem cells (MSCs) are earmarked as perfect candidatesfor cell therapy and tissue engineering due to their capacity to differentiate into different cell types. However, their potential for application in regenerative medicine declines when the levels of the reactive oxygen and nitrogen species (RONS) increase from the physiological levels, a phenomenon which is at least inevitable in ex vivo cultures and air-exposed damaged tissues. Increased levels of RONS can alter the patterns of osteogenic and adipogenic differentiation and inhibit proliferation, as well. Besides, oxidative stress enhances senescence and cell death, thus lowering the success rates of the MSC engraftment. Hence, in this review, we have selected some representatives of antioxidants and newly emerged nano antioxidants in three main categories, including chemical compounds, biometabolites, and protein precursors/proteins, which are proved to be effective in the treatment of MSCs. We will focus on how antioxidants can be applied to optimize the clinical usage of the MSCs and their associated signaling pathways. We have also reviewed several paralleled properties of some antioxidants and nano antioxidants which can be simultaneously used in real-time imaging, scaffolding techniques, and other applications in addition to their primary antioxidative function.

Iodide-doped precious metal nanoparticles: measuring oxidative stress in vivo via photoacoustic imaging.

Accumulation of reactive oxygen and nitrogen species (RONS) can induce cell damage and even cell death. RONS are short-lived species, which makes direct, precise, and real-time measurement difficult. Biologically-relevant RONS levels are in the nM-μM scale; hence, there is a need for highly sensitive RONS probes. We previously used hybrid gold-core silver-shell nanoparticles with mM sensitivity to H2O2. These particles reported the presence of RONS via spectral shifts which could easily be quantified via photoacoustic imaging. Here, we used halide doping to tune the electrochemical properties of these materials to better match the oxidation potential of RONS. This work describes the synthesis, characterization, and application of these AgI-coated gold nanorods (AgI/AuNR). The I : Ag molar ratio, pH, and initial Ag shell thickness were optimized for good RONS detection limits. Halide doping lowers the reduction potential of Ag from to resulting in a 1000-fold increase in H2O2 and 100 000-fold increase in ONOO- sensitivity. The AgI/AuNR system also etches 45-times faster than undoped Ag/AuNR. The AgI/AuNR easily reported the endogenously produced RONS in established cells lines as well as murine models.

Biochemical alterations in diclofenac-treated rats: Effect of selenium on oxidative stress, inflammation, and hematological changes

We investigated the effect of selenium (Sel), a trace element in diclofenac sodium (DCF), nonsteroidal anti-inflammatory drugs-induced hepatic and renal toxicities in adult rats. Five experimental groups namely control, DCF (10 mg/kg), Sel (0.125 mg/kg), DCF + Sel (0.125 mg/kg), and DCF + Sel (0.25 mg/kg) consisting of 10 rats each were orally treated for 7 consecutive days. Following killing, biomarkers of hepatic and renal toxicities, antioxidant enzyme levels, myeloperoxidase activity, nitric oxide levels, reactive oxygen and nitrogen species (RONS), and lipid peroxidation (LPO) were analyzed spectrophotometrically. Further, the concentration of tumor necrosis factor alpha (TNF-α) was assessed using enzyme-linked immunosorbent assay, and hematological indices: white blood cells (WBC), lymphocytes, and neutrophils and eosinophil counts. Results indicated that DCF-induced increases in biomarkers of hepatic and renal toxicity were significantly ( p < 0.05) lessened in serum of rats co-exposed to DCF and Sel in a dose-dependent manner. DCF mediated decrease in antioxidant status, and increases in RONS, LPO, and TNF-α levels were reduced ( p < 0.05) in the liver and kidney of rats co-exposed to DCF and Sel. Additionally, Sel reduced hematological abnormalities associated with DCF treatment. Light microscopic examination showed that the severity of histopathological lesions induced by DCF was lessened in rats co-exposed to DCF and Sel. Taken together, Sel supplementation mitigated DCF-induced oxidative stress, inflammation, and hematological abnormalities in the liver and kidney of treated rats.

Normobaric hyperoxia stimulates superoxide and nitric oxide production in the caudal solitary complex of rat brain slices.

Central CO2-chemosensitive neurons in the caudal solitary complex (cSC) are stimulated not only by hypercapnic acidosis, but by hyperoxia as well. While a cellular mechanism for the CO2 response has yet to be isolated, previous data show that a redox-sensitive mechanism underlies neuronal excitability to hyperoxia. However, it remains unknown how changes in Po2 affect the production of reactive oxygen and nitrogen species (RONS) in the cSC that can lead to increased cellular excitability and, with larger doses, to cellular dysfunction and death. To this end, we used fluorescence microscopy in real time to determine how normobaric hyperoxia increases the production of key RONS in the cSC. Because neurons in the region are CO2 sensitive, we also examined the potential effects of CO2 narcosis, used during euthanasia before brain slice harvesting, on RONS production. Our findings show that normobaric hyperoxia (0.4 → 0.95 atmospheres absolute O2) increases the fluorescence rates of fluorogenic dyes specific to both superoxide and nitric oxide. Interestingly, different results were seen for superoxide fluorescence when CO2 narcosis was used during euthanasia, suggesting long-lasting changes in superoxide production and/or antioxidant activity subsequent to CO2 narcosis before brain slicing. Further research needs to distinguish whether the increased levels of RONS reported here are merely increases in oxidative and nitrosative signaling or, alternatively, evidence of redox and nitrosative stress.

Endothelial Cell Redox Regulation of Ischemic Angiogenesis.

The endothelium produces and responds to reactive oxygen and nitrogen species (RONS), providing important redox regulation to the cardiovascular system in physiology and disease. In no other situation are RONS more critical than in the response to tissue ischemia. Here, tissue healing requires growth factor-mediated angiogenesis that is in part dependent on low levels of RONS, which paradoxically must overcome the damaging effects of high levels of RONS generated as a result of ischemia. Although the generation of endothelial cell RONS in hypoxia/reoxygenation is acknowledged, the mechanism for their role in angiogenesis is still poorly understood. During ischemia, the major low molecular weight thiol glutathione (GSH) reacts with RONS and protein cysteines, producing GSH-protein adducts. Recent data indicate that GSH adducts on certain proteins are essential to growth factor responses in endothelial cells. Genetic deletion of the enzyme glutaredoxin-1, which selectively removes GSH protein adducts, improves, whereas its overexpression impairs revascularization of the ischemic hindlimb of mice. Ischemia-induced GSH adducts on specific cysteine residues of several proteins, including p65 NF-kB and the sarcoplasmic reticulum calcium ATPase 2, evidently promote ischemic angiogenesis. Identifying the specific proteins in the redox response to ischemia has provided therapeutic opportunities to improve clinical outcomes of ischemia.

AMPK signaling in skeletal muscle during exercise: Role of reactive oxygen and nitrogen species

Reactive oxygen and nitrogen species (RONS) are generated during exercise depending on intensity, duration and training status. A greater amount of RONS is released during repeated high-intensity sprint exercise and when the exercise is performed in hypoxia. By activating adenosine monophosphate-activated kinase (AMPK), RONS play a critical role in the regulation of muscle metabolism but also in the adaptive responses to exercise training. RONS may activate AMPK by direct an indirect mechanisms. Directly, RONS may activate or deactivate AMPK by modifying RONS-sensitive residues of the AMPK-α subunit. Indirectly, RONS may activate AMPK by reducing mitochondrial ATP synthesis, leading to an increased AMP:ATP ratio and subsequent Thr172-AMPK phosphorylation by the two main AMPK kinases: LKB1 and CaMKKβ. In presence of RONS the rate of Thr172-AMPK dephosphorylation is reduced. RONS may activate LKB1 through Sestrin2 and SIRT1 (NAD+/NADH.H+-dependent deacetylase). RONS may also activate CaMKKβ by direct modification of RONS sensitive motifs and, indirectly, by activating the ryanodine receptor (Ryr) to release Ca2+. Both too high (hypoxia) and too low (ingestion of antioxidants) RONS levels may lead to Ser485-AMPKα1/Ser491-AMPKα2 phosphorylation causing inhibition of Thr172-AMPKα phosphorylation. Exercise training increases muscle antioxidant capacity. When the same high-intensity training is applied to arm and leg muscles, arm muscles show signs of increased oxidative stress and reduced mitochondrial biogenesis, which may be explained by differences in RONS-sensing mechanisms and basal antioxidant capacities between arm and leg muscles. Efficient adaptation to exercise training requires optimal exposure to pulses of RONS. Inappropriate training stimulus may lead to excessive RONS formation, oxidative inactivation of AMPK and reduced adaptation or even maladaptation. Theoretically, exercise programs should be designed taking into account the intrinsic properties of different skeletal muscles, the specific RONS induction and the subsequent signaling responses.

Oxidative Stress in Diabetes Mellitus

Oxidative stress is the outcome of an imbalance between the production and neutralization of reactive oxygen and nitrogen species (RONS) such that the antioxidant capacity of cell is overwhelmed. The present review briefly summarized the underlying role of overwhelming levels of RONS in the pathophysiology of diabetes mellitus (DM). The primary causative factor of oxidative stress in DM is hyperglycemia, which operates via several mechanisms. However, the individual contribution of other intermediary factors to hyperoxidative stress remains undefined, in terms of the dose response relationship between hyperglycemia and overall oxidative stress in DM. Intuitively, the inhibition and/or scavenging of intracellular free radical formation provide a therapeutic strategy to prevent oxidative stress and ensuing pathologic conditions. Therefore, the integration of antioxidants formulations into conventional therapeutic interventions, either by ingestion of natural antioxidants or through dietary supplementation, should be encouraged for a holistic approach to the management and prevention of DM and the complications associated with the pathology. Introduction Oxidative stress is the outcome of an imbalance between the production and neutralization of reactive oxygen and nitrogen species (RONS) such that the antioxidant capacity of cell is overwhelmed [1-4]. Ordinarily, the peculiar molecular configuration of oxygen (O2) confers a very slow reactivity between O2 and biomolecules. Two main factors make O2 kinetically insert; the spin restriction imposed by its triplet state, and the negative standard potential for one electron reduction of O2 to superoxide radical (O2 •−). However, O2 possesses the attributes of free radicals in that it has two unpaired electrons with parallel spin in different π-anti-bonding orbitals that is responsible for its paramagnetic properties and relative stability [4,5]. Spin restriction can be overcome by single electron exchange that converts it to strong oxidizing agent [6,7]. Therefore, the activation of O2 by specific enzymes is achieved by the presence, at the active site, of either flavins or reduced transition metals such as iron (Fe2+) and copper (Cu2+), which donates single electron to O2 [6]. In the case of metalloproteins, a varying degree of electron transfer from the metallic moiety to O2 is possible. On this basis, metalloproteins can behave either as O2 carriers (hemoglobin, hemocyanin, hemerythrin, myoglobin), where reversible interaction with O2 occurs, or as O2 reductants. Studies showed that autoxidation of oxy-hemoglobin elicit the generation of free radicals [8]. Free radical production and oxidative stress Electron transfer to O2 is catalyzed by oxidases for production of chemical energy or oxidation of substrates. These enzymes, located in different subcellular compartments (mitochondria, endoplasmic reticulum, peroxisomes) are potential sources of partially reduced Cu2+ derivatives in biological milieu. Cytosolic enzymes {xanthine oxidase, NADPH oxidases, lipoxygenase, cyclooxygenase (COX), cytochrome P450 enzymes and aldehyde oxidase}, uncoupled endothelial nitric oxide synthase (eNOS), and other hemoproteins also produce O2 •− during catalysis [2,9,10]. The mitochondrial electron transport chain reduces O2 to O2 •− at ubiquinone and NADH dehydrogenase sites whereas; microsomal cytochrome P450 and its reductases produce O2 •− during xenobiotic biotransformation [11-14]. The “leaky” inner mitochondrial membrane electron transport chain reacts with O2 directly to generate O2 •−, which dismutates to form hydrogen peroxide (H2O2), which can further react to form the hydroxyl radical ( •−OH) [2,5,10]. Additionally, the mitochondrial outer membrane enzyme monoamine oxidase catalyzes the oxidative deamination of biogenic amines and is a quantitatively large source of H2O2 that contributes to increase in the steady state concentrations of reactive species within both the mitochondrial matrix and cytosol [15]. Specifically, O2 •− is the primary radical formed by the reduction of O2 leading to secondary radicals or reactive oxygen species (ROS) such as H2O2 and •−OH in the mitochondria [2,5]. Although the cause-effect relationship remains tentative, there appears to be a strong association between mitochondrial dysfunction and chronic metabolic diseases such as Type II diabetes mellitus (T2DM) and obesity [10]. The origin, enzymatic pathways of ROS and their oxidized products, as well as their enzymatic inactivation pathways in T2DM have previously been summarized [16]. RONS have been implicated in the pathophysiology of various disease states, including diabetes mellitus (DM) and long-term development of associated complications [10,12,14,16,17]. Oxidative tissue damage is mediated byactivating a number of cellular stresssensitive pathways, which include nuclear factor-ĸB (NFĸB), p38 Correspondence to: Paul C. Chikezie, Department of Biochemistry, Imo State University, PMB 2000,Owerri, Imo State, Nigeria, Tel: +2348038935327; E-mail: p_chikezie@yahoo.com

In vitro toxicological characterisation of the S-containing arsenic metabolites thio-dimethylarsinic acid and dimethylarsinic glutathione

Inorganic arsenic is a well-documented, exposure relevant human carcinogen. A promising starting point to further understand the mechanisms behind inorganic arsenic carcinogenicity might be a formation of reactive, highly toxic metabolites during human arsenic metabolism. This study characterises the toxicity of recently identified S-containing arsenic metabolites in cultured human A549 lung adenocarcinoma epithelium cells. In direct comparison to arsenite, thio-dimethylarsinic acid (thio-DMAV) and dimethylarsinic glutathione (DMAG) exerted a 5- to 20-fold stronger cytotoxicity and showed a 2- to 20-fold higher cellular bioavailability, respectively. All three arsenicals disturbed cell cycle progression at cytotoxic concentrations, but failed to increase the level of reactive oxygen and nitrogen species (RONS) in healthy A549 cells. However, a strong disturbance of the oxidative defense system was observed after incubation with absolutely sub-cytotoxic, pico- to nanomolar concentrations of arsenite and thio-DMAV, respectively. Thus, both GSH and GSSG levels were significantly decreased by up to 40%. Accordingly, RONS levels of oxidatively (H2O2) stressed cells were strongly increased by the arsenicals. Since in vivo RONS are permanently endogenously and exogenously produced, this boost of the existing oxidative stress by arsenite and thio-DMAV might contribute to the process of inorganic arsenic induced carcinogenicity.

Hypoxia, RONS and energy metabolism in articular cartilage

Increased pro-inflammatory cytokines and reactive oxygen and nitrogen species (RONS) occur in osteoarthritis (OA). Oxygen tension can alter the levels of RONS induced by interleukin-1 (IL-1). RONS such as nitric oxide (NO) can alter energy metabolism. The aim of this study was to determine if oxygen tension alters energy metabolism, in articular cartilage, in response to IL-1 or NO and to determine if cell death occurred. Porcine articular chondrocytes were incubated with IL-1 or the NO donor NOC-18 for 48 h in either 1, 5 or 20% O(2). Adenosine triphosphate (ATP) levels were measured and immunoblots for adenosine monophosphate-activated protein kinase (AMPK) were done. Protein translation was measured by S6 activation. Senescence and autophagy were determined by increased caveolin or conversion of LC3-I to LC3-II respectively. One percent O(2) significantly reduced ATP levels compared with 20% O(2). Five percent O(2) significantly increased ATP levels compared with 20% O(2). One percent O(2) significantly increased phospho-AMPK (pAMPK) protein expression compared with 5 or 20% O(2). Oxygen tension had no effects on pS6, caveolin or LC3-II levels. IL-1-induced NO production was significantly reduced with decreased oxygen tension, and significantly reduced ATP levels at all oxygen tensions, but pAMPK was only significantly increased at 5% O(2). IL-1 significantly reduced pS6 at all oxygen tensions. IL-1 had no effects on caveolin and significantly increased LC3-II at 20% O(2) only. NOC-18 significantly reduced ATP levels at all oxygen tensions, and significantly increased pAMPK at 5% O(2) only, and significantly decreased pAMPK at 1% O(2). NOC-18 significantly reduced pS6 at 1% O(2) and significantly increased caveolin at 5% O(2), and LC3-II at 1% O(2). Our data suggest 5% O(2) is optimal for energy metabolism and protective to some effects of IL-1 and NO. NO has the greatest effects on ATP levels and the induction of autophagy at 1% O(2).

The Thioredoxin System Mediates Redox-Induced Cell Death in Human Colon Cancer Cells: Implications for the Mechanism of Action of Anticancer Agents

Anticancer agents act, at least in part, by inducing reactive oxygen and nitrogen species (RONS). We examined the redox effect on SW480 and HT-29 colon cancer cells of four anticancer compounds, arsenic trioxide, phosphoaspirin, phosphosulindac, and nitric oxide-donating aspirin (NO-ASA). All compounds inhibited the growth of both cell lines (IC(50), 10-90 micromol/L) and induced RONS detected by a general RONS molecular probe. NO-ASA, which induced at least four individual RONS (NO, H(2)O(2), superoxide anion, and peroxynitirte), induced apoptotic and necrotic cell death that was RONS-mediated (cell death paralleled RONS levels and was abrogated by N-acetyl cysteine but not by diphenylene iodonium, which displayed prooxidant activity and enhanced cell death). Nuclear factor-kappaB and mitogen-activated protein kinases were modulated by RONS. Thioredoxin-1 (Trx-1), an oxidoreductase involved in redox regulation, was heavily oxidized in response to RONS and mediated the growth inhibitory effect of the anticancer agents; knocking-down trx-1 expression by small interfering RNA abrogated cell death induced by them. These compounds also inhibited the activity of Trx reductase that reduces oxidized Trx-1, whereas the Trx reductase inhibitor aurothiomalate synergized with NO-ASA in the induction of cell death. Our findings indicate that the Trx system mediates to a large extent redox-induced cell death in response to anticancer agents. This mechanism of action may be shared by more anticancer agents and deserves further assessment as a candidate mechanism for the pharmacologic control of cancer.

Antioxidant responses in the nereidid Laeonereis acuta (Annelida, Polychaeta) after cadmium exposure

The objective of this study was to evaluate the effects of the exposure to cadmium on the antioxidant responses in the polychaeta Laeonereis acuta. The worms were submitted to 0, 5, and 100 μg of Cd/L during a period of test of 7 days. Cadmium was significantly ( p<0.05) accumulated in L. acuta in both concentrations assayed, but the concentration of reactive oxygen and nitrogen species (RONS) increased ( p<0.05) only in the group submitted to the highest concentration of cadmium (100 μg/L). At this concentration, a decrease in the activity of the superoxide dismutase and an increase of glutathione- S-transferase activity ( p<0.05) was observed. The levels of both lipid peroxides and the activities of catalase and glutathione peroxidase were not affected ( p>0.05) by the exposition to cadmium. Thus, cadmium can augment RONS levels and can interfere with the antioxidant defense system of the polychaete L. acuta, although cadmium does not directly induce oxidative stress unlike copper and iron.

Epr analysis reveals three tissues responding to endotoxin by increased formation of reactive oxygen and nitrogen species.

The excessive formation of reactive oxygen and nitrogen species (RONS) in tissue has been implicated in the development of various diseases. In this study we adopted ex vivo low temperature EPR spectroscopy combined with spin trapping technique to measure local RONS levels in frozen tissue samples. CP-H (1-hydroxy-3-carboxy-pyrrolidine), a new nontoxic spin probe, was used to analyze RONS in vivo. In addition, nitrosyl complexes of hemoglobin were determined to trace nitric oxide released into blood. By this technique we found that RONS formation in tissue of control animals increased in the following order: liver < heart < brain < cerebellum < lung < muscle < blood < ileum < kidney < duodenum < jejunum. We also found that endotoxin challenge, which represents the most common model of septic shock, increased the formation of RONS in rat liver, heart, lung, and blood, but decreased RONS formation in jejunum. We did not find changes in RONS levels in other parts of gut, brain, skeletal muscles, and kidney. Scavenging of RONS by CP-H was accompanied by an increase in blood pressure, indicating that LPS-induced vasodilatation may be due to RONS, but not due to nitric oxide. Experiments with tissue homogenates incubated in vitro with CP-H showed that ONOO(-) and O(2)(*)(-), as well as other not identified RONS, are detectable by CP-H in tissue. In summary, low-temperature EPR combined with CP-H infusion allowed detection of local RONS formation in tissues. Increased formation of RONS in response to endotoxin challenge is organ specific.