scholarly journals Multiple isoforms of mitochondrial glutathione S-transferases and their differential induction under oxidative stress

2002 ◽  
Vol 366 (1) ◽  
pp. 45-55 ◽  
Author(s):  
Haider RAZA ◽  
Marie-Anne ROBIN ◽  
Ji-kang FANG ◽  
Narayan G. AVADHANI
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Peptide Mapping ◽  
Mitochondrial Respiratory Chain ◽  
Immunoblot Analysis ◽  
Liver Mitochondria ◽  
Membrane Lipid ◽  
Dependent Manner ◽  
Mitochondrial Oxidative Stress ◽  
Mitochondrial Glutathione

The mitochondrial respiratory chain, which consumes approx. 85–90% of the oxygen utilized by cells, is a major source of reactive oxygen species (ROS). Mitochondrial genetic and biosynthetic systems are highly susceptible to ROS toxicity. Intramitochondrial glutathione (GSH) is a major defence against ROS. In the present study, we have investigated the nature of the glutathione S-transferase (GST) pool in mouse liver mitochondria, and have purified three distinct forms of GST: GSTA1-1 and GSTA4-4 of the Alpha family, and GSTM1-1 belonging to the Mu family. The mitochondrial localization of these multiple GSTs was confirmed using a combination of immunoblot analysis, protease protection assay, enzyme activity, N-terminal amino acid sequencing, peptide mapping and confocal immunofluorescence analysis. Additionally, exogenously added 4-hydroxynonenal (HNE), a reactive byproduct of lipid peroxidation, to COS cells differentially affected the cytosolic and mitochondrial GSH pools in a dose- and time-dependent manner. Our results show that HNE-mediated mitochondrial oxidative stress caused a decrease in the GSH pool, increased membrane lipid peroxidation, and increased levels of GSTs, glutathione peroxidase and Hsp70 (heat-shock protein 70). The HNE-induced oxidative stress persisted for longer in the mitochondrial compartment, where the recovery of GSH pool was slower than in the cytosolic compartment. Our study, for the first time, demonstrates the presence in mitochondria of multiple forms of GSTs that show molecular properties similar to those of their cytosolic counterparts. Our results suggest that mitochondrial GSTs may play an important role in defence against chemical and oxidative stress.

scholarly journals Preclinical Study on the Ameliorating Effect of L-Ascorbic Acid for the Oxidative Stress of Caused by Chronic Administration of Organic Nitrates in Cardiovascular Diseases

2021 ◽  
Author(s):  
Ahmed M Hamdan ◽  
Zuhair M. Mohammedsaleh ◽  
Aalaa Aboelnour ◽  
Sherif M.H. Elkhannishi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Chronic Administration ◽  
Stress Factors ◽  
Male Rats ◽  
Oxidative Stress Marker ◽  
Organic Nitrates ◽  
Dependent Manner ◽  
Dose Dependent

Abstract PurposeThe therapeutic activity of Glyceryl trinitrate (GTN) is mainly regulated by liberating nitric oxide (NO) and reactive nitrogen species (RNS). During this biotransformation, oxidative stress and lipid peroxidation inside the red blood cells (RBCs) occur. The principal objective of our research is to explain the ameliorating effect of L-ascorbic acid for the deleterious effects of chronic administration of nitrovasodilator drugs. MethodsWe studied some biochemical parameters for the oxidative stress using groups of high sucrose/fat (HSF) diet Wistar male rats chronically orally administered ISMN. Afterwards, we evaluated the role of L-ascorbic acid against these biochemical changes. ResultsChronic treatment with organic nitrates caused elevated serum levels of lipid peroxidation, hemoglobin derivatives as methemoglobin and carboxyhemoglobin, rate of hemoglobin autoxidation, the cellular levels of pro-inflammatory cytokines marker (NF-κB) and apoptosis markers (caspase-3) in myocardium muscles in a dose dependent manner. Meanwhile, such exposure caused decline in the enzymatic effect of superoxide dismutase (SOD), glutathione (GSH) and catalase activity (CAT) accompanied with a decrease of in the level of mitochondrial oxidative stress marker (nrf2) in myocardium muscles and decrease in the serum iron and total iron binding capacity (TIBC) in a dose dependent manner. Concomitant treatment with L-ascorbic acid significantly diminished these changes for all examined parameters.ConclusionChronic administration of organic nitrates leads to the alteration of the level of oxidative stress factors in the myocardium tissue due to generation of reactive oxygen species. Using vitamin C can effectively ameliorate such intoxication to overcome the nitrate tolerance.

scholarly journals Antioxidant and Anti-inflammatory Protective Properties of Thai Shallot (Allium ascalonicum cv. Chiangmai) Juice on Human Vascular Endothelial Cell Lines (EA.hy926)

2019 ◽  
Vol 16 (3) ◽  
pp. 175-184
Author(s):  
Sakaewan OUNJAIJEAN ◽  
Sukanya CHACHIYO ◽  
Kanokwan KULPRACHAKARN ◽  
Kongsak BOONYAPRANAI ◽  
Somdet SRICHAIRATANAKOOL ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Membrane Lipid ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Ros Production ◽  
Food Ingredient ◽  
Human Vascular Endothelial Cell ◽  
Anti Inflammatory

Oxidative stress and inflammation are 2 major contributors to numerous life-threatening disorders, including vascular pathologies. Shallots (Allium ascalonicum) are a type of red onion which grows in Southeast Asia. Bulbs of this plant are used both as a food ingredient and in traditional medicine. This study attempted to investigate the possible ways that juice extracted from Thai shallot (A.ascalonicum cv. Chiangmai) bulbs could be used in the prevention of cardiovascular complications. The antioxidative and anti-inflammatory effects of shallot juice extract (SHE) on human vascular endothelial cells (EA.hy926) were investigated. Cell viability was evaluated by MTT assay, membrane lipid peroxidation by thiobarbituric acid reactive substances assay, intracellular reactive oxygen species (ROS) production by the fluorescent probe 6-carboxy-2'-7'-dichlorofluoresceine, and interleukin-6 (IL-6) released by ELISA. The shallot juice showed extremely low cytotoxicity against EA.hy926 cells, with IC50 of 41.9 and 27.3 mg/ml for 24 h- and 48 h-incubation, respectively. SHE reduced the iron-induced malondialdehyde production in a dose-dependent manner. The extract also demonstrated antioxidant activity as shown by a significant reduction of H2O2-induced ROS production at a low concentration (< 200 mg/ml). Furthermore, SHE significantly attenuated the level of IL-6 released during lipopolysaccharide stimulation (p < 0.05). It is of interest that the juice extracted from Thai shallot bulbs demonstrated both cellular antioxidant and anti-inflammatory properties in endothelial cell models, combined with a reduction in toxicity. Shallot extract could be considered as a nutraceutical for the prevention or management of vascular diseases as it is related to oxidative stress and inflammation.

scholarly journals Antioxidant activity of pineal methoxyindoles on hepatocyte plasmatic membrane

2019 ◽  
Vol 2 (1) ◽  
pp. 161-174
Author(s):  
Marcos C Reyes-Gonzales ◽  
Eduardo Esteban-Zubero ◽  
Laura López-Pingarrón ◽  
María Soledad Soria ◽  
Desiree Pereboom ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Membrane ◽  
Membrane Fluidity ◽  
Membrane Lipid ◽  
Hydroxyl Group ◽  
Dependent Manner ◽  
Protective Effects ◽  
Concentration Dependent Manner ◽  
Plasmatic Membrane ◽  
Membrane Rigidity

Antioxidant effect of several pineal derived molecules has been well documented. Here, the protective effects of 5-methoxytryptophol (5-MTOH) and 5-methoxyindol-3-acetic acid (5-MIAA) on hepatic cell membrane lipid peroxidation and cell membrane rigidity induced by FeCl3 plus ascorbic acid have been systemically investigated. The membrane fluidity was evaluated by fluorescence spectroscopy, malondialdehyde (MDA) and 4-hydroxyalkenals (4-HDA) concentrations and carbonyl groups of protein were measured as the parameters of lipid and protein damage, respectively. Results showed that oxidative stress increased membrane rigidity, MDA and 4-HDA concentrations as well as carbonyl content in a concentration-dependent manner. 5-MTOH, but not 5-MIAA, significantly attenuated these oxidative indecies. In absence of oxidative stress, none of these methoxyindoleamines modified the content of MDA, 4-HDA or carbonylation. However 5-MIAA at its highest concentration slightly modified membrane fluidity. The results suggest that structural modification of C3 in the methoxyindoleamine, that is, the carboxyl group replaced by hydroxyl group in this site could improve the ability of 5-methoxyindoleamine derivatives to preserve membrane fluidity of cells which are under oxidative stress. 

scholarly journals Role of Membrane Lipid Peroxidation, Enzymatic and Non-enzymatic Antioxidative Systems in the Development of Chilling Injury in Japanese Plums

2012 ◽  
Vol 137 (6) ◽  
pp. 473-481 ◽  
Author(s):  
Sukhvinder Pal Singh ◽  
Zora Singh
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cold Storage ◽  
Chilling Injury ◽  
Membrane Lipid ◽  
Enzymatic Antioxidants ◽  
Membrane Lipid Peroxidation ◽  
Stress Theory ◽  
Antioxidative Systems ◽  
Duration Of Storage

Chilling injury (CI) is a major postharvest constraint in the long-term cold storage, transportation, and distribution of japanese plums (Prunus salicina). The aim of the work was to explain the development and severity of CI in japanese plums based on the oxidative stress theory following time course analysis of enzymatic and non-enzymatic antioxidants. Changes in membrane lipid peroxidation and enzymatic and non-enzymatic antioxidative systems in japanese plum cultivar Blackamber were determined at weekly intervals during 5 weeks of cold storage at 0 °C and at 2-day intervals during poststorage simulated shelf conditions (21 ± 1 °C) for 8 days after each week of cold storage. Fruit respiration and ethylene production rates showed typical climacteric patterns after removal from cold storage and these rates were relatively high after 4 and 5 weeks compared with 0 to 3 weeks of storage. The CI symptoms first appeared after 3 weeks of cold storage after fruit had been transferred to simulated shelf conditions. The incidence and severity of CI intensified with increasing storage duration. The extent of lipid peroxidation indicated by concentration of thiobarbituric acid-reactive substances and membrane damage manifested as electrolyte leakage increased with increasing duration of storage and subsequent simulated shelf conditions. Membrane lipid peroxidation exhibited positive correlation with the severity of CI. Activities of primary antioxidant enzymes and the enzymes involved in the ascorbate–glutathione cycle were determined to explain the levels of reduced and oxidized forms of cellular redox buffers, ascorbate and glutathione. In response to chilling stress, antioxidative protection systems operated efficiently during the first 3 weeks of cold storage, but extended storage resulted in loss of ability to ameliorate increasing levels of oxidative stress. In this study, the comprehensive analyses of various metabolites and antioxidative systems explain the series of events involved in development of CI in japanese plums in support of the oxidative stress theory.

Trigonella foenum-graecumprotection against deltamethrin-induced toxic effects on haematological, biochemical, and oxidative stress parameters in rats

2014 ◽  
Vol 92 (8) ◽  
pp. 679-685 ◽  
Author(s):  
Mohamed M. Abdel-Daim ◽  
Mabrouk A. Abd Eldaim ◽  
Mohamed M. Mahmoud
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Mass ◽  
Biochemical Parameters ◽  
Toxic Effects ◽  
Protective Agent ◽  
Dependent Manner ◽  
Hematological And Biochemical Parameters ◽  
Trigonella Foenum Graecum L ◽  
And Oxidative Stress

Trigonella foenum-graecum L. is enriched with many active ingredients. TFG oil was evaluated for its protective effect against deltamethrin toxicity in rats. Rats of the control group were administered saline. The 2nd group was administered deltamethrin (DLM) orally at a concentration of 15 mg/kg body mass. The 3rd and 4th groups were administered DLM at a concentration of 15 mg/kg body mass and were fed diets containing 2.5% and 5% TFG oil, respectively. DLM intoxication reduced red blood cell and platelet counts, hemoglobin concentration, and hematocrit value while it induced leucocytosis. Furthermore, it increased serum levels of lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, γ-glutamyltransferase, triglycerides, cholesterol, uric acid, urea, and creatinine; increased hepatic, renal, and brain lipid peroxidation; decreased serum acetylcholine esterase level; and decreased hepatic, renal, and brain antioxidant markers’ activities. However, TFG oil kept the studied hematological and biochemical parameters within normal ranges. In addition, it prevented lipid peroxidation and oxidative stress induced by DLM intoxication in a dose-dependent manner. Therefore, these results indicated that TFG oil inhibited the toxic effects of DLM on hematological and biochemical parameters as well as oxidative status by its free radical scavenging and potent antioxidant activities, and it appeared to be a promising protective agent against DLM-induced toxicity.

scholarly journals Cobalt Chloride Alters Mitochondrial Function in a Dose Dependent Manner

2021 ◽  
Vol 37 (3) ◽  
Author(s):  
Pham Thi Bich ◽  
Vu Thi Thu
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Cobalt Chloride ◽  
Dose Dependence ◽  
Cell Counting ◽  
Dependent Manner ◽  
Mitochondrial Oxidative Stress ◽  
H9c2 Cardiomyocytes ◽  
Dose Dependent

Aim: This study was carried to evaluates of Cobalt chloride (CoCl2) on cardiac mitochondrial function. Methods: H9C2 cardiomyocytes were cultured in medium containing different concentrations of CoCl2. Cell viability, cardiolipin content, mitochondrial function, and mitochondrial oxidative stress were assessed by using Cell Counting Kit-8 and suitable fluorescence kits. Results: The obtained data showed that CoCl2 (200÷400 µM) induced cell death and decreased mitochondrial function of H9C2 cardiomyocytes in dose dependence. Especially, CoCl2 at dose of 300 µM significantly altered values of mitochondrial membrane potential, H2O2 and O2- to 63.79±2.15%, 145.81±5.83% and 143.10±3.07% (of 100% control), respectively. Conclusion: CoCl2 strongly induced cardiomyocyte death via altering mitochondrial function in a dose-dependent manner.

scholarly journals The flavonoids, quercetin and isorhamnetin 3-O-acylglucosides diminish neutrophil oxidative metabolism and lipid peroxidation.

2001 ◽  
Vol 48 (1) ◽  
pp. 183-189 ◽  
Author(s):  
M Zielińska ◽  
A Kostrzewa ◽  
E Ignatowicz ◽  
J Budzianowski
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Metabolism ◽  
Hypochlorous Acid ◽  
Thiobarbituric Acid ◽  
Membrane Lipid ◽  
Polymorphonuclear Neutrophils ◽  
Inhibitory Influence ◽  
Dependent Manner ◽  
In Vitro Production

Two natural flavonoids, quercetin and isorhamnetin 3-O-acylglucosides, were examined for their inhibitory influence on the in vitro production and release of reactive oxygen species in polymorphonuclear neutrophils (PMNs). The generation of superoxide radical, hydrogen peroxide and hypochlorous acid were measured by, respectively, cytochrome c reduction, dichlorofluorescin oxidation and taurine chlorination. Membrane lipid oxidation was studied by the thiobarbituric acid method in mouse spleen microsomes. The addition of flavonoids at the concentration range 1-100 microM inhibited PMNs oxidative metabolism and lipid peroxidation in a dose-dependent manner. The results suggest that these flavonoids suppress the oxidative burst of PMNs and protect membranes against lipid peroxidation.

scholarly journals Oxidative Stress of Vanadium-Mediated Oxygen Free Radical Generation Stimulated by Aluminium on Human Erythrocytes

1998 ◽  
Vol 35 (2) ◽  
pp. 254-260 ◽  
Author(s):  
M A M Abou-Seif
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Osmotic Fragility ◽  
Thiobarbituric Acid ◽  
Oxygen Free Radical ◽  
Membrane Lipid ◽  
Human Erythrocytes ◽  
Membrane Lipid Peroxidation ◽  
Radical Generation

It has been suggested that aluminium stimulates vanadium-mediated superoxide radical generation. The oxidative stress of generated superoxide radicals on antioxidant enzyme activity, oxidation of NADH and NADPH, membrane lipid peroxidation and osmotic fragility in human red blood cells (RBC) was investigated. RBC were incubated with varying concentrations of vanadium and aluminium ions at 37°C for 2 h. RBC incubated with vanadium ions showed significantly increased superoxide dismutase and catalase activities, and oxidized NADH and NADPH concentrations compared with control RBC preparations. Erythrocyte lipid peroxidation was assessed by measuring thiobarbituric acid reactivity. RBC incubated with elevated levels of vanadium showed significantly increased membrane lipid peroxidation when compared with control RBC; it increased further on addition of aluminium. A significant positive correlation was observed between the extent of vanadium induced membrane lipid peroxidation and the osmotic fragility of treated RBC. In the presence of vanadium, aluminium stimulates superoxide dismutase and catalase activities, NADH and NADPH oxidation and membrane lipid peroxidation, as well as increasing osmotic fragility of human erythrocytes. The stimulatory effect of aluminium was dependent on concentration. These results may have implications for the mechanism of toxicity of aluminium and vanadium in haemodialysis patients.

Abstract 526: 4-hydroxy-2-nonenal (HNE), a Lipid Peroxidation Product, Exerts Both Pro- and Anti-thrombotic Effects on Vascular Cells

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Hema Kothari ◽  
Rit Vatsyayan ◽  
Vijaya Mohan Rao
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Procoagulant Activity ◽  
Dependent Manner ◽  
Lipid Peroxidation Product ◽  
Vascular Cells ◽  
Tnf Α ◽  
Activation Assay

Background: Oxidative stress and generation of lipid peroxidation (LPO) products are detrimental in the pathogenesis of atherosclerosis and associated acute thrombotic events. However, recent studies suggest that moderate oxidative stress and low levels of LPO products can induce adaptive immune responses and exert beneficial effects. Tissue factor (TF) is a critical initiator of coagulation and aberrant TF expression on vascular cells under inflammation triggers intravascular thrombosis. HNE, a highly reactive LPO product and TF have been shown to be associated with atherosclerosis. Recently, we demonstrated that HNE decrypts procoagulant activity of pre-existing TF on activated monocytes and endothelial cells and generates TF+ microparticles. Here, we investigated the effect of HNE on induction of TF and cell adhesion molecules in monocytes and endothelial cells that were not perturbed earlier. Methods and results: THP-1 monocytic cells and endothelial cells (HUVEC) were stimulated with LPS and TNF-α/IL1-β, respectively, in the presence of a control vehicle or varying concentrations of HNE that are pathophysiologically relevant. TF induction was measured at mRNA (by qRT-PCR), protein (by immunoblotting) and activity levels (in factor X activation assay). Pre-treating cells with HNE inhibited TNF-α/IL1-β- or LPS-stimulated TF procoagulant activity in a dose-dependent manner. THP-1 and HUVEC varied in their sensitivities to HNE (THP-1> HUVEC). HNE-mediated inhibition of TF activity correlated with lower TF mRNA and protein levels. Our results demonstrate that HNE prevents TNF-α/IL1-β- and LPS-induced IKKβ degradation and thereby inhibits NFκβ activation. In addition to inhibiting TF expression, HNE significantly reduced monocyte adhesion to endothelial cells through downregulating TNF-α/IL1-β-induced expression of endothelial adhesion molecules VCAM-1 and ICAM-1. Conclusion: HNE may play a dual role in regulating TF activity in atherosclerosis. HNE could act as a prothrombotic mediator by increasing coagulant activity of pre-existing TF through decryption process. HNE can also elicit anti-thrombotic and anti-inflammatory effect by inhibiting TF and adhesion molecules in response to stimulus by impairing the NF-ĸB pathway.

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