scholarly journals Reactive Oxygen Species, Lipid Peroxidation and Antioxidative Defense Mechanism

2013 ◽  
Vol 41 (1) ◽  
pp. 44 ◽  
Author(s):  
Hossam S. EL-BELTAGI ◽  
Heba I. MOHAMED
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Carbonyl Compounds ◽  
Defense Mechanism ◽  
Lipid Peroxides ◽  
Cellular Injury ◽  
Oxygen Species ◽  
Antioxidative Defense ◽  
Inhibit Lipid Peroxidation ◽  
Reactive Carbonyl Compounds

Lipid peroxidation can be defined as the oxidative deterioration of lipids containing any number of carbon-carbon double bonds. Lipid peroxidation is a well-established mechanism of cellular injury in both plants and animals, and is used as an indicator of oxidative stress in cells and tissues. Lipid peroxides are unstable and decompose to form a complex series of compounds including reactive carbonyl compounds. The oxidation of linoleates and cholesterol is discussed in some detail. Analytical methods for studying lipid peroxidation were mentioned. Various kinds of antioxidants with different functions inhibit lipid peroxidation and the deleterious effects caused by the lipid peroxidation products.

scholarly journals Antioxidative defense mechanism of the ruderal Verbascum olympicum Boiss. against copper (Cu)-induced stress

2016 ◽  
Vol 11 (1) ◽  
pp. 10-20 ◽  
Author(s):  
Ayşegül Uğar Akpınar ◽  
Hülya Arslan ◽  
Gürcan Güleryüz ◽  
Serap Kırmızı
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Defense Mechanism ◽  
Growth Parameters ◽  
Antioxidative Defense ◽  
Membrane Injury ◽  
Induced Stress ◽  
Hoagland Nutrient Solution ◽  
Hydroponic Conditions

AbstractThe endemic Verbascum olympicum has characteristics that allows it to live in degraded areas of Uludağ Mountain, Turkey and therefore known as a ruderal species. In this study, V. olympicum seeds collected from Uludağ Mountain were grown in the Hoagland nutrient solution, under hydroponic conditions. The activity of antioxidative enzymes (superoxide dismutase, SOD; catalase, CAT; ascorbate peroxidase, APX) were examined to demonstrate the role of antioxidative mechanism in the seedlings exposed to different Cu concentrations (0, 50, 250, 500 μM) for seven days. Also, certain growth parameters (such as the water content, biomass production, soluble protein), the level of lipid peroxidation, cell membrane injury and permeability were investigated. As a result, some toxic effects are observed following the application of 500 μM Cu, after the seedlings growing in 50 and 250 mM Cu concentrations showed high resistance and survived in hydroponic conditions. Our findings provide information about the resistance of V. Olympicum seedlings to oxidative stress caused by excessive Cu concentrations.

scholarly journals Oxidative Stress Level in the Testes of Mice and Rats during Nickel Intoxication

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Eugenia Murawska-Ciałowicz ◽  
Wojciech Bal ◽  
Lidia Januszewska ◽  
Marcin Zawadzki ◽  
Joanna Rychel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Stress Level ◽  
Reduced Glutathione ◽  
Redox Balance ◽  
Oxygen Species ◽  
Antioxidative Defense ◽  
Carcinogenic Effect ◽  
Oxidative Stress Level

The genotioxic and carcinogenic effect of nickel probably results from its capacity to produce reactive oxygen species (ROS) and disturb the redox balance. The aim of the study was to find out if rats lacking spermatic protamine 2 are less susceptible to Ni(II) than mice. Consequently, the levels of malondialdehyde + 4 hydroxynonenal (MDA+4HDA) − markers of lipid peroxidation, as well as the level of reduced glutathione (GSH) were measured within the rat and mouse testes. Our results showed that the levels of lipid peroxidation markers were elevated in testicular homogenates of intoxicated mice without any changes in rats. GSH level was lower in the group of intoxicated mice comparing to the control without statistically significant changes in rats’ homogenates. Moreover, the level of GSH in the testes of intoxicated mice was lower than in rats. On the basis of our results, it appears that Ni(II) can initiate oxidative stress in the testes of mice but not of rats and can reduce GSH level. Consequently, the antioxidative defense of the testes is reduced. Ni(II) that causes oxidative stress in the testes may also contribute to infertility.

scholarly journals Ginkgo biloba extract (EGb 761) attenuates oxidative stress induction in erythrocytes of sickle cell disease patients

2012 ◽  
Vol 48 (4) ◽  
pp. 659-665 ◽  
Author(s):  
Aline Emmer Ferreira Furman ◽  
Railson Henneberg ◽  
Priscila Bacarin Hermann ◽  
Maria Suely Soares Leonart ◽  
Aguinaldo José do Nascimento
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Sickle Cell ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Intracellular Reactive Oxygen Species ◽  
Oxygen Species ◽  
Egb 761 ◽  
Cell Disease

Sickle cell disease promotes hemolytic anemia and occlusion of small blood vessels due to the presence of high concentrations of hemoglobin S, resulting in increased production of reactive oxygen species and decreased antioxidant defense capacity. The aim of this study was to evaluate the protective action of a standardized extract of Ginkgo biloba (EGb 761), selected due to its high content of flavonoids and terpenoids, in erythrocytes of patients with sickle cell anemia (HbSS, SS erythrocytes) subjected to oxidative stress using tert-butylhydroperoxide or 2,2-azobis-(amidinepropane)-dihydrochloride, in vitro. Hemolysis indexes, reduced glutathione, methemoglobin concentrations, lipid peroxidation, and intracellular reactive oxygen species were determined. SS erythrocytes displayed increased rates of oxidation of hemoglobin and membrane lipid peroxidation compared to normal erythrocytes (HbAA, AA erythrocytes), and the concentration of EGb 761 necessary to achieve the same antioxidant effect in SS erythrocytes was at least two times higher than in normal ones, inhibiting the formation of intracellular reactive oxygen species (IC50 of 13.6 µg/mL), partially preventing lipid peroxidation (IC50 of 242.5 µg/mL) and preventing hemolysis (IC50 of 10.5 µg/mL). Thus, EGb 761 has a beneficial effect on the oxidative status of SS erythrocytes. Moreover, EGb 761 failed to prevent oxidation of hemoglobin and reduced glutathione at the concentrations examined.

scholarly journals Oxidative Stress and Carbonyl Lesions in Ulcerative Colitis and Associated Colorectal Cancer

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Zhiqi Wang ◽  
Sai Li ◽  
Yu Cao ◽  
Xuefei Tian ◽  
Rong Zeng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Ulcerative Colitis ◽  
Carbonyl Compounds ◽  
Gene Mutations ◽  
Oxygen Species ◽  
Inflammatory Conditions ◽  
Dna Mutations ◽  
Pathogenic Factors ◽  
Protein Dysfunction

Oxidative stress has long been known as a pathogenic factor of ulcerative colitis (UC) and colitis-associated colorectal cancer (CAC), but the effects of secondary carbonyl lesions receive less emphasis. In inflammatory conditions, reactive oxygen species (ROS), such as superoxide anion free radical (O2∙-), hydrogen peroxide (H2O2), and hydroxyl radical (HO∙), are produced at high levels and accumulated to cause oxidative stress (OS). In oxidative status, accumulated ROS can cause protein dysfunction and DNA damage, leading to gene mutations and cell death. Accumulated ROS could also act as chemical messengers to activate signaling pathways, such as NF-κB and p38 MAPK, to affect cell proliferation, differentiation, and apoptosis. More importantly, electrophilic carbonyl compounds produced by lipid peroxidation may function as secondary pathogenic factors, causing further protein and membrane lesions. This may in turn exaggerate oxidative stress, forming a vicious cycle. Electrophilic carbonyls could also cause DNA mutations and breaks, driving malignant progression of UC. The secondary lesions caused by carbonyl compounds may be exceptionally important in the case of host carbonyl defensive system deficit, such as aldo-keto reductase 1B10 deficiency. This review article updates the current understanding of oxidative stress and carbonyl lesions in the development and progression of UC and CAC.

Different Chilling-Induced Symptoms and the Underlying Oxidative Stress and Antioxidative Defense in the Exocarp and Mesocarp of Immature Sponge Gourd (Luffa cylindrica) Fruit

2021 ◽  
Author(s):  
Pichaya Chuenchom ◽  
Sompoch Noichinda ◽  
Kitti Bodhipadma ◽  
Chalermchai Wongs-Aree ◽  
David W. M. Leung
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Considerable Increase ◽  
Chilling Injury ◽  
Oxygen Species ◽  
Antioxidative Defense ◽  
Sponge Gourd ◽  
Lower Temperature ◽  
High Level ◽  
The Relationship

Immature sponge gourd fruit is consumed as a vegetable with a limited shelf life. Although cold storage is a simple and powerful tool for maintaining postharvest fruit quality, storage at a low temperature may not be appropriate for vegetables as some chilling injury (CI) of the immature sponge gourd fruit may occur. Therefore, this research aimed to elucidate the relationship between CI, oxidative stress, and the antioxidative defense mechanisms in the exocarp and mesocarp of immature sponge gourd fruit. After storage at 5°C for 6 days, visual CI symptoms, including browning and surface pitting, were found in the peel (exocarp) but not in the mesocarp. There were, however, more dead cells (stained by Evans blue) in the mesocarp of the fruit stored at 5°C. There was a more considerable increase in the electrolyte leakage rate in both fruit tissues held at 5°C than 25°C. The CI was correlated with malondialdehyde (MDA) levels in the tissues. The MDA of fruit exocarp at 5°C was 1.6 fold higher than that at 25°C on day 6, while the lipoxygenase (LOX) activity in mesocarp was 50% higher in fruit stored at a lower temperature. The action of ascorbate peroxidase (APX) was high in the exocarp of the fruit stored at 5°C, but there appeared to be a continuous depletion of the co-substrate or ascorbic acid. In conclusion, the CI in the exocarp was mainly associated with a high level of reactive oxygen species (ROS). In contrast, the CI in the mesocarp appeared to be primarily associated with increased lipid peroxidation by the elevated LOX activity under cold stress compared to storage at 25°C.

Intrathymic and intrasplenic oxidative stress mediates thymocyte and splenocyte damage in acutely exercised mice

1999 ◽  
Vol 86 (6) ◽  
pp. 1823-1827 ◽  
Author(s):  
A. A. Azenabor ◽  
L. Hoffman-Goetz
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Acute Exercise ◽  
Lipid Peroxides ◽  
Membrane Lipid ◽  
Splenic Tissue ◽  
Lymphoid Tissues ◽  
Oxygen Species ◽  
The Impact

Reactive oxygen species may contribute to apoptosis in lymphoid tissues observed after exercise. Thymic and splenic tissues excised from control mice (C) or mice immediately after ( t 0) or 24 h after ( t 24) a run to exhaustion (RTE) were assayed for biochemical indexes of oxidative stress [thymic and splenic membrane lipid peroxides, superoxide dismutase, catalase, plasma uric acid (UA), and ascorbic acid (AA)]. There were significant increases in membrane lipid peroxides in thymus ( P < 0.001) and spleen ( P < 0.001) in acutely exercised mice relative to controls (thymus: C = 2.74 ± 0.80 μM; t 0 = 7.45 ± 0.48 μM; t 24 = 9.44 ±1.41 μM; spleen: C = 0.48 ± 0.22 μM; t 0 = 1.78 ± 0.28 μM; t 24 = 2.81 ± 0.34 μM). The thymic and splenic tissue antioxidant enzymes concentrations of superoxide dismutase and catalase were significantly lower in samples collected at t 0 relative to C and t 24 mice ( P < 0.001). Plasma UA and AA levels were used to assess the impact of the RTE on the peripheral antioxidant pool. There was no significant change in UA levels and a significant reduction in plasma AA concentrations ( P < 0.001); the reduction in plasma AA occurred at t 24 (6.53 ± 1.64 μM) relative to t 0 (13.11 ± 0.71 μM) and C (13.26 ± 1.2 μM). These results suggest that oxidative damage occurs in lymphoid tissues after RTE exercise and that such damage may contribute to lymphocyte damage observed after acute exercise.

scholarly journals DHA reduces oxidative stress following hypoxia-ischemia in newborn piglets: a study of lipid peroxidation products in urine and plasma

2018 ◽  
Vol 46 (2) ◽  
pp. 209-217 ◽  
Author(s):  
Marianne Ullestad Huun ◽  
Håvard T. Garberg ◽  
Javier Escobar ◽  
Consuelo Chafer ◽  
Maximo Vento ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Oxygen Species ◽  
Major Contributor ◽  
Time Points ◽  
Newborn Piglets ◽  
Hypoxia Group ◽  
Hypoxia Ischemia ◽  
Anti Oxidant

AbstractBackground:Lipid peroxidation mediated by reactive oxygen species is a major contributor to oxidative stress. Docosahexaenoic acid (DHA) has anti-oxidant and neuroprotective properties. Our objective was to assess how oxidative stress measured by lipid peroxidation was modified by DHA in a newborn piglet model of hypoxia-ischemia (HI).Methods:Fifty-five piglets were randomized to (i) hypoxia, (ii) DHA, (iii) hypothermia, (iv) hypothermia+DHA or (v) sham. All groups but sham were subjected to hypoxia by breathing 8% O2. DHA was administered 210 min after end of hypoxia and the piglets were euthanized 9.5 h after end of hypoxia. Urine and blood were harvested at these two time points and analyzed for F4-neuroprostanes, F2-isoprostanes, neurofuranes and isofuranes using UPLC-MS/MS.Results:F4-neuroprostanes in urine were significantly reduced (P=0.006) in groups receiving DHA. Hypoxia (median, IQR 1652 nM, 610–4557) vs. DHA (440 nM, 367–738, P=0.016) and hypothermia (median, IQR 1338 nM, 744–3085) vs. hypothermia+DHA (356 nM, 264–1180, P=0.006). The isoprostane compound 8-iso-PGF2α was significantly lower (P=0.011) in the DHA group compared to the hypoxia group. No significant differences were found between the groups in blood.Conclusion:DHA significantly reduces oxidative stress by measures of lipid peroxidation following HI in both normothermic and hypothermic piglets.

Serine proteases increase oxidative stress in lung cells

2001 ◽  
Vol 281 (3) ◽  
pp. L556-L564 ◽  
Author(s):  
Kazutetsu Aoshiba ◽  
Kimihiko Yasuda ◽  
Shuji Yasui ◽  
Jun Tamaoki ◽  
Atsushi Nagai
Keyword(s):  
Oxidative Stress ◽  
Serine Proteases ◽  
Direct Interaction ◽  
Lung Fibroblasts ◽  
Lung Cells ◽  
Cellular Injury ◽  
Oxygen Species ◽  
Cytotoxic Effects ◽  
Bronchial Epithelial ◽  
High Concentrations

Several serine proteases are directly cytotoxic. We investigated whether the cytotoxic effects of proteases are associated with increased levels of reactive oxygen species (ROS) in cells. We found that treatment of lung fibroblasts or bronchial epithelial cells with relatively high concentrations (0.1–100 U/ml) of neutrophil elastase, trypsin, and Pronase increased ROS levels in the mitochondria and cytoplasm. The protease-induced increase in ROS was associated with oxidative cellular injury as determined by generation of 8-hydroxy-2′-deoxyguanosine and malonaldehyde plus 4-hydroxyalkenal. The protease-induced increase in ROS was not merely due to cell detachment because the proteases also caused an increase in ROS in suspended cells, which precluded attachment to the extracellular matrix. The protease-induced increase in ROS appears to contribute to cytotoxicity because cell death induced by proteases was attenuated by treatment with catalase, a decomposer of H2O2, and accelerated by treatment with aminotriazole, a catalase inhibitor. These results suggest that several proteases increase oxidative stress, indicating a direct interaction between proteases and ROS in mediating cytotoxicity.

scholarly journals Research Strategies in the Study of the Pro-Oxidant Nature of Polyphenol Nutraceuticals

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Harvey Babich ◽  
Alyssa G. Schuck ◽  
Jeffrey H. Weisburg ◽  
Harriet L. Zuckerbraun
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Copper Ions ◽  
Oxygen Species ◽  
Research Strategies ◽  
Dual Nature ◽  
Intracellular Glutathione ◽  
Divalent Cobalt ◽  
Per Se

Polyphenols of phytochemicals are thought to exhibit chemopreventive effects against cancer. These plant-derived antioxidant polyphenols have a dual nature, also acting as pro-oxidants, generating reactive oxygen species (ROS), and causing oxidative stress. When studying the overall cytotoxicity of polyphenols, research strategies need to distinguish the cytotoxic component derived from the polyphenolper sefrom that derived from the generated ROS. Such strategies include (a) identifying hallmarks of oxidative damage, such as depletion of intracellular glutathione and lipid peroxidation, (b) classical manipulations, such as polyphenol exposures in the absence and presence of antioxidant enzymes (i.e., catalase and superoxide dismutase) and of antioxidants (e.g., glutathione andN-acetylcysteine) and cotreatments with glutathione depleters, and (c) more recent manipulations, such as divalent cobalt and pyruvate to scavenge ROS. Attention also must be directed to the influence of iron and copper ions and to the level of polyphenols, which mediate oxidative stress.

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