Oxidative Modification of Enzymes During Aging and Acute Oxidative Stress

1988 ◽  
pp. 537-540 ◽  
Author(s):  
Pamela E. Starke-Reed ◽  
Cynthia N. Oliver
Keyword(s):  
Oxidative Stress ◽  
Oxidative Modification

scholarly journals Antioxidants, lysosomes and elements status during the life cycle of sea trout Salmo trutta m. trutta L.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Natalia Kurhaluk ◽  
Halyna Tkachenko
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Muscle Tissue ◽  
Salmo Trutta ◽  
Protein Carbonyl ◽  
Oxidative Modification ◽  
Oxidative Stress Biomarkers ◽  
Development Stages ◽  
Stress Biomarkers ◽  
Element Contents

AbstractThe aim of our study was to elucidate the effects of both development stages (parr, smolt, adult, spawner), and kelt as a survival form and sex (male, female) on the functional stability of the lysosomal complex, biomarkers of oxidative stress, and element contents in the muscle tissue of the sea trout (Salmo trutta m. trutta L.) sampled in the Pomerania region (northern Poland). We have evaluated the maximal activities of lysosomal enzymes (alanyl aminopeptidase, leucyl aminopeptidase, β-N-acetylglucosaminidase, and acid phosphatase), lipid peroxidation level, and protein carbonyl derivatives as indices of muscle tissue degradation. The relationship between lysosomal activity and oxidative stress biomarkers estimated by the lipid peroxidation level and protein carbonyl derivatives was also assessed, as well as the relationships between element levels and oxidative stress biomarkers. Trends of the main effects (i.e., the development stages and sex alone, the interaction of the sex and development stage simultaneously) on oxidative stress biomarkers, lysosomal functioning, and element contents in the muscle tissue were evaluated. The study has shown sex-related relationships between the pro- and antioxidant balance and the tissue type in the adult stage as well as modifications in the lysosomal functioning induced by long-term environmental stress associated with changing the habitats from freshwater to seawater and intense migrations. The highest level of toxic products generated in oxidative reactions and oxidative modification of proteins was noted in both the spawner stage and the kelt form. The holistic model of analysis of all parameters of antioxidant defense in all development stages and sex demonstrated the following dependencies for the level of lipid peroxidation, oxidative modification of proteins, lysosomal activities, and element contents: TBARS > OMP KD > OMP AD > TAC, AcP > NAG > LAP > AAP and Cu > Fe > Ca > Mn > Zn > Mg, respectively.

Rescue of anaemia and autoimmune responses in SOD1-deficient mice by transgenic expression of human SOD1 in erythrocytes

2009 ◽  
Vol 422 (2) ◽  
pp. 313-320 ◽  
Author(s):  
Yoshihito Iuchi ◽  
Futoshi Okada ◽  
Rina Takamiya ◽  
Noriko Kibe ◽  
Satoshi Tsunoda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Energy Charge ◽  
Reactive Oxygen ◽  
Oxidative Modification ◽  
Autoimmune Response ◽  
Oxygen Species ◽  
Autoantibody Production ◽  
Deficient Mice ◽  
Human Sod1

Oxidative stress has been implicated as a cause of various diseases such as anaemia. We found that the SOD1 [Cu,Zn-SOD (superoxide dismutase)] gene deficiency causes anaemia, the production of autoantibodies against RBCs (red blood cells) and renal damage. In the present study, to further understand the role of oxidative stress in the autoimmune response triggered by SOD1 deficiency, we generated mice that had the hSOD1 (human SOD1) transgene under regulation of the GATA-1 promoter, and bred the transgene onto the SOD1−/− background (SOD1−/−;hSOD1tg/+). The lifespan of RBCs, levels of intracellular reactive oxygen species, and RBC content in SOD1−/−;hSOD1tg/+ mice, were approximately equivalent to those of SOD1+/+ mice. The production of antibodies against lipid peroxidation products, 4-hydroxy-2-nonenal and acrolein, as well as autoantibodies against RBCs and carbonic anhydrase II were elevated in the SOD1−/− mice, but were suppressed in the SOD1−/−;hSOD1tg/+ mice. Renal function, as judged by blood urea nitrogen, was improved in the transgenic mice. These results rule out the involvement of a defective immune system in the autoimmune response of SOD1-deficient mice, because SOD1−/−;hSOD1tg/+ mice carry the hSOD1 protein only in RBCs. Metabolomic analysis indicated a shift in glucose metabolism to the pentose phosphate pathway and a decrease in the energy charge potential of RBCs in SOD1-deficient mice. We conclude that the increase in reactive oxygen species due to SOD1 deficiency accelerates RBC destruction by affecting carbon metabolism and increasing oxidative modification of lipids and proteins. The resulting oxidation products are antigenic and, consequently, trigger autoantibody production, leading to autoimmune responses.

scholarly journals Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies

Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1645
Author(s):  
Bart De Geest ◽  
Mudit Mishra
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Gene Therapy ◽  
Steady State ◽  
Gene Transfer ◽  
Oxidative Modification ◽  
Heme Oxygenase 1 ◽  
Therapy Studies ◽  
Pathological Remodeling

Under physiological circumstances, there is an exquisite balance between reactive oxygen species (ROS) production and ROS degradation, resulting in low steady-state ROS levels. ROS participate in normal cellular function and in cellular homeostasis. Oxidative stress is the state of a transient or a persistent increase of steady-state ROS levels leading to disturbed signaling pathways and oxidative modification of cellular constituents. It is a key pathophysiological player in pathological hypertrophy, pathological remodeling, and the development and progression of heart failure. The heart is the metabolically most active organ and is characterized by the highest content of mitochondria of any tissue. Mitochondria are the main source of ROS in the myocardium. The causal role of oxidative stress in heart failure is highlighted by gene transfer studies of three primary antioxidant enzymes, thioredoxin, and heme oxygenase-1, and is further supported by gene therapy studies directed at correcting oxidative stress linked to metabolic risk factors. Moreover, gene transfer studies have demonstrated that redox-sensitive microRNAs constitute potential therapeutic targets for the treatment of heart failure. In conclusion, gene therapy studies have provided strong corroborative evidence for a key role of oxidative stress in pathological remodeling and in the development of heart failure.

Indicator Characterizing Carbonyl-Dependent Modification of Erythrocytic Superoxydismutase as a Biochemical Marker of Oxidative Stress in Coronary Heart Disease

Kardiologiia ◽  
2020 ◽  
Vol 60 (5) ◽  
pp. 57-61
Author(s):  
A. K. Tikhaze ◽  
V. Ya. Kosach ◽  
V. Z. Lankin ◽  
A. A. Panferova ◽  
M. D. Smirnova
Keyword(s):  
Oxidative Stress ◽  
Heart Disease ◽  
Stress Intensity ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Oxidative Modification ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Sod Activity ◽  
Stress Marker

Aim To study the oxidative modification of red blood cell Cu,Zn superoxide dismutase (SOD) in patients with ischemic heart disease (IHD) in vivo and in vitro to substantiate the use of a new oxidative stress marker.Material and methods Red blood cell Cu,Zn SOD was measured by depression of nitrotetrazolium blue reduction by the superoxide anion generated in xanthine oxidase xanthine oxidation. Red blood cell Cu,Zn SOD was measured immunochemically. The biochemical study was performed in the control group (patients with low extremity fracture without known history of cardiovascular diseases and hyperlipidemia) and in groups of patients with acute myocardial infarction, stable angina, and decompensated heart failure. For evaluation of oxidative stress intensity in IHD patients, an empirical SOD oxidative modification coefficient (OMCSOD) was proposed, which is a Cu,Zn SOD activity / Cu,Zn SOD content ratio.Results The red blood cell Cu,Zn SOD activity was significantly decreased in all IHD groups compared to the control group. Furthermore, OMCSOD was also considerably decreased in IHD patients, which warrants the use of this biochemical index as an oxidative stress marker.Conclusion It was shown that the Cu,Zn SOD modification was induced by interaction of the enzyme molecules with a natural dicarbonyl, malonic dialdehyde, and OMCSOD can be used for evaluation of oxidative stress intensity in IHD patients.

scholarly journals Reducing sugars trigger oxidative modification and apoptosis in pancreatic β-cells by provoking oxidative stress through the glycation reaction

1996 ◽  
Vol 320 (3) ◽  
pp. 855-863 ◽  
Author(s):  
Hideaki KANETO ◽  
Junichi FUJII ◽  
Theingi MYINT ◽  
Nobuko MIYAZAWA ◽  
Kazi N. ISLAM ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Cleavage ◽  
Reducing Sugars ◽  
Islet Cells ◽  
Chromatin Condensation ◽  
Oxidative Modification ◽  
Lipid Peroxidation Product ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Peroxidation Product

Several reducing sugars brought about apoptosis in isolated rat pancreatic islet cells and in the pancreatic β-cell-derived cell line HIT. This apoptosis was characterized biochemically by internucleosomal DNA cleavage and morphologically by nuclear shrinkage, chromatin condensation and apoptotic body formation. N-Acetyl-l-cysteine, an antioxidant, and aminoguanidine, an inhibitor of the glycation reaction, inhibited this apoptosis. We also showed directly that proteins in β-cells were actually glycated by using an antibody which can specifically recognize proteins glycated by fructose, but not by glucose. Furthermore, fluorescence-activated cell sorting analysis using dichlorofluorescein diacetate showed that reducing sugars increased intracellular peroxide levels prior to the induction of apoptosis. Levels of carbonyl, an index of oxidative modification, and of malondialdehyde, a lipid peroxidation product, were also increased. Taken together, these results suggest that reducing sugars trigger oxidative modification and apoptosis in pancreatic β-cells by provoking oxidative stress mainly through the glycation reaction, which may explain the deterioration of β-cells under conditions of diabetes.

scholarly journals SERCA activity is reduced in DJ-1 mutant flies and human cells due to oxidative modification

2020 ◽  
Author(s):  
Cristina Solana-Manrique ◽  
Verónica Muñoz-Soriano ◽  
Francisco José Sanz ◽  
Nuria Paricio
Keyword(s):  
Oxidative Stress ◽  
Human Cell ◽  
Protein Function ◽  
Therapeutic Strategies ◽  
Oxidative Modification ◽  
Pharmacological Intervention ◽  
Post Translational Modification ◽  
Causative Gene ◽  
Functional Link ◽  
Familial Parkinson’S Disease

ABSTRACTDJ-1 is a causative gene for familial Parkinson’s disease (PD) with different functions, standing out its role against oxidative stress (OS). Accordingly, PD model flies harboring a mutation in the DJ-1β gene (the Drosophila ortholog of human DJ-1) show high levels of OS markers like protein carbonylation, a common post-translational modification that may alter protein function. To increase our understanding of PD pathogenesis as well as to discover potential therapeutic targets for pharmacological intervention, we performed a redox proteomic assay in DJ-1β mutant flies. Among the proteins that showed increased carbonylation levels in PD model flies, we found SERCA, an endoplasmic reticulum Ca2+ channel that plays an important role in Ca2+ homeostasis. Several studies have supported the involvement of Ca2+ dyshomeostasis in PD. Interestingly, a functional link between DJ-1 and Ca2+ homeostasis maintenance was previously reported. Thus, we decided to study the relation between SERCA activity and PD physiopathology. Our results showed that SERCA enzymatic activity is significantly reduced in DJ-1β mutant flies, probably as a consequence of OS-induced carbonylation, as well as in a human cell PD model based on DJ-1-deficiency. Indeed, higher carbonylation levels of SERCA were also observed in DJ-1-deficient SH-SY5Y neuron-like cells compared to controls. In addition, we demonstrated that SERCA activity was increased in both PD models after treatment with a specific activator of this protein, CDN1163. Consistently, CDN1163 was also able to restore PD-related phenotypes in PD model flies and to increase viability in the human cell PD model. Taken together, our results indicate that impaired SERCA activity in both familial PD models may play a role in PD physiopathology. In addition, we demonstrate that therapeutic strategies addressing SERCA activation could be beneficial to treat this disease as shown for CDN1163.

scholarly journals The effect of biguanide derivatives on oxidative stress in rats with hyperglycemia

2018 ◽  
Vol 64 (3) ◽  
pp. 261-267
Author(s):  
E.I. Gorina ◽  
T.N. Popova ◽  
K.K. Shulgin ◽  
S.S. Popov ◽  
L.F. Panchenko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Dna Fragmentation ◽  
Reduced Glutathione ◽  
Conjugated Dienes ◽  
Oxidative Modification ◽  
Regulatory Effect ◽  
Glutathione Antioxidant System ◽  
Primary Products ◽  
Radical Processes

The effect of the synthetic biguanide derivatives N-[imino(1-piperidinyl)methyl]guanidine (NIPMG) and 1,3-dimethyl-5-[(carbamimidamidomethanimidoil) amino]benzoyl-1,3dicarboxylate (DCB) on the degree of proteins oxidative modification (POM) and the DNA fragmentation, the content of the lipid peroxidation primary products – conjugated dienes (CD), and the activity of glutathione antioxidant system in the liver and heart of rats with experimental hyperglycemia was investigated. Administration of the biguanides (15.0 mg/kg) to hypoglycemic rats promoted reduction of the free radical processes intensity in the studied tissues. Data about CD and POM level changes in hyperglycemic rats treated by NIPMG and DKB correlate with the results of DNA fragmentation degree evaluation. At the same time, the activity of antioxidant enzymes (glutathione peroxidase and glutathione reductase), and the reduced glutathione content in the liver and heart of rats changed toward control values. For metformin, which was used as a comparison drug, changes in the studied parameters in the same direction were also found. These results indicate the ability of the tested biguanide derivatives to exhibit a positive regulatory effect on free radical homeostasis, reducing the degree of oxidative stress at this pathology.

scholarly journals The influence of oxidized fibrinogen on apoptosis of endothelial cells

2011 ◽  
Vol 57 (2) ◽  
pp. 210-218 ◽  
Author(s):  
A.V. Aseychev ◽  
O.A. Azizova ◽  
O.N. Scheglovitova ◽  
N.N. Sklyankina ◽  
G.G. Borisenko
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Death ◽  
Critical Role ◽  
Vascular Diseases ◽  
Oxidative Modification ◽  
Cell Protection ◽  
Oxidized Fibrinogen ◽  
Atherosclerosis Development ◽  
Cardio Vascular

Oxidative stress plays an important role in cardio-vascular diseases and atherosclerosis. Fibrinogen (FB), plasma coagulation protein, is a risk factor of atherosclerosis. Importantly, it can be readily oxidized during oxidative stress and in pathological conditions. FB can promote angiogenesis by supporting migration and proliferation of endothelial cells. On the other hand, recent reports demonstrated cytotoxicity of oxidized fibrinogen (oxFB). Endothelial dysfunction plays a critical role in the atherosclerosis development, therefore it is important to understand the effect of oxFB on human endothelial cells (hEC), and the mechanism of the cell death. Here, we studied influence of oxFB on hEC during 24 h incubation in two conditions: (1) at low serum level (0.1%) and in the absence of growth factors ("starvation"); (2) in full medium (5% FBS) with growth factor supplement. Apoptosis was evaluated using analysis of nuclear morphology, phosphatidylserine externalization on hEC surface and caspase-3 activation. In starvation, we observed significant cell death via apoptosis. FB prevented starvation-induced cell death and caspase activation. Caspase activity in the presence of oxFB was 1.5 times higher as compared to FB, yet oxFB demonstrated significant cell protection during stress. Similarly, in optimal cultivation conditions FB decreased the rate of apoptosis by three times, while oxFB supported cell viability to the lesser extent. Thus, FB can protect hEC in stress conditions (in starvation); oxidative modification of FB diminishes its antiapoptotic properties.

scholarly journals THE IMPACT OF METFORMIN AND ROSUVASTATIN ON THE MARKERS OF OXIDATIVE STRESS, GLYCEMIC CONTROL, AND LIPID PROFILE IN RATS WITH STREPTOZOTOCIN-NICOTINAMIDE-INDUCED DIABETES AFTER ACUTE INTRACEREBRAL HEMORRHAGE

2021 ◽  
Vol 78 (4) ◽  
pp. 87-93
Author(s):  
Volodymyr Zhyliuk ◽  
Anton Lievykh ◽  
Alla Shevtsova ◽  
Vitaliy Mamchur ◽  
Viktoriia Tkachenko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Glycemic Control ◽  
Intracerebral Hemorrhage ◽  
Lipid Profile ◽  
Positive Control ◽  
Negative Control ◽  
Oxidative Modification ◽  
Markers Of Oxidative Stress ◽  
The Impact

Hyperproduction of highly active carbonyl compounds and reactive oxygen species initiates the development of oxidative stress in various pathological conditions and protein carbonylation is considered to be one of the key factors in the progression of diabetes mellitus and associated complications. This comparative research aimed to study the effect of metformin and rosuvastatin on the levels of biochemical markers of oxidative stress, glycemic control, and lipid profile in rats with type 2 diabetes mellitus (T2DM) complicated by a brain hemorrhage.T2DM was simulated with a single intraperitoneal injection of nicotinamide and streptozotocin (NA/STZ) to male Wistar rats (n=38). Intracerebral hemorrhage (ICH) was induced by microinjection of 1 μL of bacterial collagenase 0.2 IU/μL into the striatum. Animals were randomized into 5 groups: negative control, intact rats; positive control 1, NA/STZ; positive control 2, NA/STZ+ICH; metformin, 250 mg/kg +NA/STZ+ICH; rosuvastatin, 15 mg/kg+NA/STZ+ICH. Drug effects were assessed by the area under the glycemic curve (AUC), the content of glucose, glycated hemoglobin (HbA1c), total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL), homocysteine (Hcy), advanced glycation end products (AGEs), and the markers of oxidative modification of proteins – aldehyde- and ketonephenylhydrazones (APH/KPH) in blood serum.It was found that brain hemorrhage in rats with T2DM can intensify the manifestations of oxidative modification of molecules and worsen glycemic control and lipid profile. Under these conditions, rosuvastatin improved lipid metabolism and reduced the levels of AGEs by 35.1% but did not affect glycemia and content of APH/KPH. Metformin reduced oxidative stress (AGEs by 35.4%, KPH by 21.2%) as well as improved both glycemic status and lipid profile (TG level by 20.2%, TG/HDL ratio by 31.9%). Both drugs did not produce any effect on Hcy level.Thus, metformin in conditions of T2DM complicated by acute ICH has advantages over rosuvastatin in relation to the markers of oxidative modification and glycemic control.

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