scholarly journals Effect of Natural Food Antioxidants Against LDL and DNA Oxidative Changes

2018 ◽  
Author(s):  
Sotirios Kiokias ◽  
Charalampos Proestos ◽  
Vassilki Oreopoulou
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Review Paper ◽  
Oxidative Modification ◽  
Natural Food ◽  
Antioxidant Compounds ◽  
Oxygen Species ◽  
Radical Oxygen Species ◽  
Dna Oxidative Damage

Radical oxygen species formed in human tissue cells by many endogenous and exogenous pathways, cause extensive oxidative damage, which has been linked to various human diseases. This review paper provides an overview of lipid peroxidation and focuses on the free-radicals initiated processes of LDL oxidative modification and DNA oxidative damage, which are widely associated to the initiation and development of atherosclerosis and carcinogenesis, respectively. The article subsequently provides an overview of the recent human trials or even in vitro investigations on the potential of natural antioxidant compounds (such as carotenoids, vitamins C and E) to monitor LDL and DNA oxidative changes.

scholarly journals Effect of Natural Food Antioxidants against LDL and DNA Oxidative Changes

Antioxidants ◽  
2018 ◽  
Vol 7 (10) ◽  
pp. 133 ◽  
Author(s):  
Sotirios Kiokias ◽  
Charalampos Proestos ◽  
Vassilki Oreopoulou
Keyword(s):  
Oxidative Damage ◽  
Review Paper ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Oxidative Modification ◽  
Natural Food ◽  
Antioxidant Compounds ◽  
Radical Oxygen Species ◽  
Dna Oxidative Damage

Radical oxygen species formed in human tissue cells by many endogenous and exogenous pathways cause extensive oxidative damage which has been linked to various human diseases. This review paper provides an overview of lipid peroxidation and focuses on the free radicals-initiated processes of low-density lipoprotein (LDL) oxidative modification and DNA oxidative damage, which are widely associated with the initiation and development of atherosclerosis and carcinogenesis, respectively. The article subsequently provides an overview of the recent human trials or even in vitro investigations on the potential of natural antioxidant compounds (such as carotenoids; vitamins C and E) to monitor LDL and DNA oxidative changes.

scholarly journals Tetrandrine Attenuated Doxorubicin-Induced Acute Cardiac Injury in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Gang Li ◽  
Wen-Rui Li ◽  
Ya-Ge Jin ◽  
Qi-Qiang Jie ◽  
Cheng-Yu Wang ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Cardiac Function ◽  
Cardiac Injury ◽  
Whole Body ◽  
Oxygen Species ◽  
Single Intraperitoneal Injection ◽  
Body Wasting ◽  
Nrf2 Expression

Oxidative damage is closely involved in the development of doxorubicin- (DOX-) induced cardiotoxicity. It has been reported that tetrandrine can prevent the development of cardiac hypertrophy by suppressing reactive oxygen species- (ROS-) dependent signaling pathways in mice. However, whether tetrandrine could attenuate DOX-related cardiotoxicity remains unclear. To explore the protective effect of tetrandrine, mice were orally given a dose of tetrandrine (50 mg/kg) for 4 days beginning one day before DOX injection. To induce acute cardiac injury, the mice were exposed to a single intraperitoneal injection of DOX (15 mg/kg). The data in our study showed that tetrandrine prevented DOX-related whole-body wasting and heart atrophy, decreased markers of cardiac injury, and improved cardiac function in mice. Moreover, tetrandrine supplementation protected the mice against oxidative damage and myocardial apoptotic death. Tetrandrine supplementation also reduced ROS production and improved cell viability after DOX exposure in vitro. We also found that tetrandrine supplementation increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) expression and activity in vivo and in vitro. The protection of tetrandrine supplementation was blocked by Nrf2 deficiency in mice. In conclusion, our study found that tetrandrine could improve cardiac function and prevent the development of DOX-related cardiac injury through activation of Nrf2.

scholarly journals Formation of Oxidatively Modified Lipids as the Basis for a Cellular Epilipidome

2020 ◽  
Vol 11 ◽  
Author(s):  
Corinne M. Spickett
Keyword(s):  
Biological Effects ◽  
Oxidative Modification ◽  
Oxygen Species ◽  
Radical Oxygen Species ◽  
Chemical Mechanisms ◽  
Control Gene Expression ◽  
Lipid Species ◽  
Regulatory Effects ◽  
Oxidatively Modified ◽  
The Stability

While often regarded as a subset of metabolomics, lipidomics can better be considered as a field in its own right. While the total number of lipid species in biology may not exceed the number of metabolites, they can be modified chemically and biochemically leading to an enormous diversity of derivatives, many of which retain the lipophilic properties of lipids and thus expand the lipidome greatly. Oxidative modification by radical oxygen species, either enzymatically or chemically, is one of the major mechanisms involved, although attack by non-radical oxidants also occurs. The modified lipids typically contain more oxygens in the form of hydroxyl, epoxide, carbonyl and carboxylic acid groups, and nitration, nitrosylation, halogenation or sulfation can also occur. This article provides a succinct overview of the types of species formed, the reactive compounds involved and the specific molecular sites that they react with, and the biochemical or chemical mechanisms involved. In many cases, these modifications reduce the stability of the lipid, and breakdown products are formed, which themselves have interesting properties such as the ability to react with other biomolecules. Publications on the biological effects of modified lipids are growing rapidly, supporting the concept that some of these biomolecules have potential signaling and regulatory effects. The question therefore arises whether modified lipids represent an “epilipidome”, analogous to the epigenetic modifications that can control gene expression.

scholarly journals Silicon Alleviates Copper Toxicity in Flax Plants by Up-Regulating Antioxidant Defense and Secondary Metabolites and Decreasing Oxidative Damage

2020 ◽  
Vol 12 (11) ◽  
pp. 4732 ◽  
Author(s):  
Hossam S. El-Beltagi ◽  
Mahmoud R. Sofy ◽  
Mohammed I. Aldaej ◽  
Heba I. Mohamed
Keyword(s):  
Lipid Peroxidation ◽  
Plant Growth ◽  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Growth Yield ◽  
Enzymatic Antioxidants ◽  
Oxygen Species ◽  
Total Chlorophyll ◽  
Yield Attributes ◽  
Cu Toxicity

In recent years, nutrient management has gained much attention as a way to mitigate heavy metal stress. Silicon (Si) promotes plant defense responses against toxic metal stresses. In this study, we evaluated the effects of silicon (Si) on copper (Cu) toxicity in two flax genotypes (Sakha 1 and Sakha 2) as it relates to plant growth, yield attributes, total chlorophyll, nucleic acid content, enzymatic and non-enzymatic antioxidants, oxidative damage, lipid peroxidation, copper and silicon content, and fatty acid composition. The results showed that Cu (100 and 200 µM) inhibited plant growth and increased Cu accumulation in soil, roots, and shoots. Cu significantly decreased the yield attributes, total chlorophyll by 9.5% and 22% in Sakha 1 and by 22.5% and 29% in Sakha 2, and enhanced the accumulation of non-enzymatic (tocopherol), enzymatic antioxidants such as superoxide dismnutase, peroxidase, ascorbate peroxidase and catalase) and secondary metabolites (phenol and flavonoids). The DNA content significantly decreased in stressed plants with 100 and 200 µM Cu about 22% and 44%, respectively, in Sakha 1 and about 21.6% and 34.7% in Sakha 2, and RNA content also decreased by about 20% and 29%, respectively, in Sakha 1 and by about 2% and 13% in Sakha 2 compared to the control plant. Furthermore, Cu stress accelerated the generation of reactive oxygen species (ROS), such as hydrogen peroxide (H2O2) and induced cellular oxidative injury caused by lipid peroxidation. In parallel, Cu induced a change in the composition of fatty acids, resulting in lower unsaturated fatty acid levels and increased saturated fatty acids (increased saturation/unsaturation ratio for both genotypes). Treating the flax plants with irrigation three times with Si protected the plants from Cu toxicity. Si treatment decreased the uptake and the transport of Cu to the shoots and harvested seeds and promoted plant growth, yield attributes, and antioxidant defense systems by reducing Cu accumulation, lipid peroxidation, and the generation of H2O2. In addition, the alleviation of Cu toxicity correlated with increased Si accumulation in the roots and shoots. In conclusion, Si can be used to improve the resistance of flax plants to Cu toxicity by up-regulating the antioxidant defense system such as superoxide dismutase (SOD), peroxidase (POD), ascorbate peroxidase (APX) and catalase (CAT) and decreasing the oxidative damage caused by reactive oxygen species (ROS).

scholarly journals Ultraendurance exercise increases the production of reactive oxygen species in isolated mitochondria from human skeletal muscle

2010 ◽  
Vol 108 (4) ◽  
pp. 780-787 ◽  
Author(s):  
Kent Sahlin ◽  
Irina G. Shabalina ◽  
C. Mikael Mattsson ◽  
Linda Bakkman ◽  
Maria Fernström ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Vastus Lateralis ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Work Intensity ◽  
Isolated Mitochondria ◽  
Mitochondrial Ros

Exercise-induced oxidative stress is important for the muscular adaptation to training but may also cause muscle damage. We hypothesized that prolonged exercise would increase mitochondrial production of reactive oxygen species (ROS) measured in vitro and that this correlates with oxidative damage. Eight male athletes (24–32 yr) performed ultraendurance exercise (kayaking/running/cycling) with an average work intensity of 55% V̇o2peak for 24 h. Muscle biopsies were taken from vastus lateralis before exercise, immediately after exercise, and after 28 h of recovery. The production of H2O2 was measured fluorometrically in isolated mitochondria with the Amplex red and peroxidase system. Succinate-supported mitochondrial H2O2 production was significantly increased after exercise (73% higher, P = 0.025) but restored to the initial level at recovery. Plasma level of free fatty acids (FFA) increased fourfold and exceeded 1.2 mmol/l during the last 6 h of exercise. Plasma FFA at the end of exercise was significantly correlated to mitochondrial ROS production ( r = 0.74, P < 0.05). Mitochondrial content of 4-hydroxy-nonenal-adducts (a marker of oxidative damage) was increased only after recovery and was not correlated with mitochondrial ROS production. Total thiol group level and glutathione peroxidase activity were elevated after recovery. In conclusion, ultraendurance exercise increases ROS production in isolated mitochondria, but this is reversed after 28 h recovery. Mitochondrial ROS production was not correlated with oxidative damage of mitochondrial proteins, which was increased at recovery but not immediately after exercise.

Oxidative stress-related responses of Bifidobacterium longum subsp. longum BBMN68 at the proteomic level after exposure to oxygen

Microbiology ◽  
2011 ◽  
Vol 157 (6) ◽  
pp. 1573-1588 ◽  
Author(s):  
Man Xiao ◽  
Pan Xu ◽  
Jianyun Zhao ◽  
Zeng Wang ◽  
Fanglei Zuo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Bifidobacterium Longum ◽  
Transcriptional Level ◽  
Low Oxygen ◽  
Oxygen Stress ◽  
Dna Oxidative Damage ◽  
Proteomic Approach ◽  
Protective Proteins

Bifidobacterium longum subsp. longum BBMN68, an anaerobic probiotic isolated from healthy centenarian faeces, shows low oxygen (3 %, v/v) tolerance. To understand the effects of oxidative stress and the mechanisms protecting against it in this strain, a proteomic approach was taken to analyse changes in the cellular protein profiles of BBMN68 under the following oxygen-stress conditions. Mid-exponential phase BBMN68 cells grown in MRS broth at 37 °C were exposed to 3 % O2 for 1 h (I) or 9 h (II), and stationary phase cells were subjected to 3 % O2 for 1 h (III). Respective controls were grown under identical conditions but were not exposed to O2. A total of 51 spots with significant changes after exposure to oxygen were identified, including the oxidative stress-protective proteins alkyl hydroperoxide reductase C22 (AhpC) and pyridine nucleotide-disulfide reductase (PNDR), and the DNA oxidative damage-protective proteins DNA-binding ferritin-like protein (Dps), ribonucleotide reductase (NrdA) and nucleotide triphosphate (NTP) pyrophosphohydrolases (MutT1). Changes in polynucleotide phosphorylase (PNPase) plus enolase, which may play important roles in scavenging oxidatively damaged RNA, were also found. Following validation at the transcriptional level of differentially expressed proteins, the physiological and biochemical functions of BBMN68 Dps were further proven by in vitro and in vivo tests under oxidative stress. Our results reveal the key oxidative stress-protective proteins and DNA oxidative damage-protective proteins involved in the defence strategy of BBMN68 against oxygen, and provide the first proteomic information toward understanding the responses of Bifidobacterium and other anaerobes to oxygen stress.

scholarly journals Therapeutic Potential of Polar and Non-Polar Extracts ofCyanthillium cinereum In Vitro

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Gunjan Guha ◽  
V. Rajkumar ◽  
R. Ashok Kumar ◽  
Lazar Mathew
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Oxidative Damage ◽  
Therapeutic Potential ◽  
Reducing Power ◽  
Total Phenolic ◽  
Xtt Assay ◽  
Polar Extracts ◽  
Scavenging Efficiency

Cyanthillium cinereum(Less.) H. Rob. (Asteraceae) has been traditionally known for its medicinal properties, all aspects of which are yet to be exploited. This study was aimed at investigating the therapeutic potential of polar (methanolic and aqueous) and nonpolar (hexane and chloroform) crude extracts of the whole plant. Several parameters including free-radical (DPPH•, ABTS•+, H2O2and•OH) scavenging, reducing power, protection of DNA against oxidative damage, cytotoxicity, inhibition of oxidative hemolysis in erythrocytes, total phenolic content and inhibition of lipid peroxidation were examined. All the free-radical generating assay models demonstrated positive scavenging efficiency with differential but considerable magnitudes for the four extracts. However, only the hexane extract showed significant H2O2scavenging effect. Lipid peroxidation was estimated by thiobarbituric acid-malondialdehyde (MDA) reaction, and a high degree of inhibition was shown by all the extracts. Reducing power of the polar extracts was higher than the non-polar ones. All extracts showed a concentration-dependent increase in phenolic contents. Oxidative damage to erythrocytes was hindered by all extracts in diverse degrees. XTT assay showed that all extracts have mild cytotoxic property. The aqueous extract evidently demonstrated protective effect on pBR322 plasmid DNA against oxidative breakdown. These results suggested the potential ofC. cinereumas medicine against free-radical-associated oxidative damage and related degenerative diseases involving metabolic stress, genotoxicity and cytotoxicity.

The protective ability of Mediterranean dietary plants against the oxidative damage: The role of radical oxygen species in inflammation and the polyphenol, flavonoid and sterol contents

2009 ◽  
Vol 112 (3) ◽  
pp. 587-594 ◽  
Author(s):  
Filomena Conforti ◽  
Silvio Sosa ◽  
Mariangela Marrelli ◽  
Federica Menichini ◽  
Giancarlo A. Statti ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Oxygen Species ◽  
Radical Oxygen Species ◽  
Protective Ability ◽  
Dietary Plants

scholarly journals Pyridoxine Decreases Oxidative Stress on Human Erythrocyte Membrane Protein in vitro

2019 ◽  
Vol 13 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Margarita Velásquez ◽  
Darío Méndez ◽  
Carlos Moneriz
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Membrane Protein ◽  
Oxidative Damage ◽  
Erythrocyte Membrane ◽  
Cumene Hydroperoxide ◽  
Protein Carbonylation ◽  
Human Erythrocytes ◽  
Red Cell Membrane

Background: Pyridoxine has reduction and prevention against the levels of reactive oxygen species in in vitro studies. However, the biochemical mechanism that explains this behavior has not yet been fully clarified. Objective: To evaluate the effect of pyridoxine against oxidative damage on the membrane of human erythrocytes. Methods: Cumene hydroperoxide was used to induce oxidative stress in protein and lipid. Human erythrocytes were incubated with pyridoxine and cumene hydroperoxide, either alone or together for 8 h. Oxidative damage was determined by measuring lipid peroxidation and membrane protein carbonylation. Results: The results indicate that the malondialdehyde concentration decreased with increasing concentration of pyridoxine. The membrane protein content also decreased with increasing concentration of vitamin B6, which was confirmed by the decreased signal intensity in the western blot when compared to control without pyridoxine. Results demonstrate that pyridoxine can significantly decrease lipid peroxidation and protein carbonylation in red cell membrane exposed to high concentrations of oxidant agent. Conclusion: Pyridoxine showed a protective effect against the oxidative stress in human erythrocytes in vitro, inhibiting the carbonylation and the oxidative damage of erythrocyte membrane proteins. To date, such an effect has not yet been reported in terms of protein oxidation.

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