Peroxidase-Catalyzed Oxidative Damage of DNA and 2‘-Deoxyguanosine by Model Compounds of Lipid Hydroperoxides:  Involvement of Peroxyl Radicals

2000 ◽  
Vol 13 (12) ◽  
pp. 1199-1207 ◽  
Author(s):  
Waldemar Adam ◽  
Annemarie Kurz ◽  
Chantu R. Saha-Möller
Keyword(s):  
Oxidative Damage ◽  
Peroxyl Radicals ◽  
Lipid Hydroperoxides ◽  
Model Compounds

scholarly journals Dietary Supplementation with the MicroalgaGaldieria sulphuraria(Rhodophyta) Reduces Prolonged Exercise-Induced Oxidative Stress in Rat Tissues

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Simona Carfagna ◽  
Gaetana Napolitano ◽  
Daniela Barone ◽  
Gabriele Pinto ◽  
Antonino Pollio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Acute Exercise ◽  
Ischemia Reperfusion ◽  
Dietary Supplementation ◽  
Peroxyl Radicals ◽  
Antioxidant Enzyme Activities ◽  
Rat Tissues ◽  
Lipid Hydroperoxides ◽  
Exercise Induced

We studied the effects of ten-day 1%Galdieria sulphurariadietary supplementation on oxidative damage and metabolic changes elicited by acute exercise (6-hour swimming) determining oxygen consumption, lipid hydroperoxides, protein bound carbonyls in rat tissue (liver, heart, and muscle) homogenates and mitochondria, tissue glutathione peroxidase and glutathione reductase activities, glutathione content, and rates of H2O2mitochondrial release. Exercise increased oxidative damage in tissues and mitochondria and decreased tissue content of reduced glutathione. Moreover, it increased State 4 and decreased State 3 respiration in tissues and mitochondria.G. sulphurariasupplementation reduced the above exercise-induced variations. Conversely, alga supplementation was not able to modify the exercise-induced increase in mitochondrial release rate of hydrogen peroxide and in liver and heart antioxidant enzyme activities. The alga capacity to reduce lipid oxidative damage without reducing mitochondrial H2O2release can be due to its high content of C-phycocyanin and glutathione, which are able to scavenge peroxyl radicals and contribute to phospholipid hydroperoxide metabolism, respectively. In conclusion,G. sulphurariaability to reduce exercise-linked oxidative damage and mitochondrial dysfunction makes it potentially useful even in other conditions leading to oxidative stress, including hyperthyroidism, chronic inflammation, and ischemia/reperfusion.

scholarly journals Interactions of peroxynitrite with human plasma and its constituents: oxidative damage and antioxidant depletion

1994 ◽  
Vol 303 (1) ◽  
pp. 295-301 ◽  
Author(s):  
A Van der Vliet ◽  
D Smith ◽  
C A O'Neill ◽  
H Kaur ◽  
V Darley-Usmar ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Ascorbic Acid ◽  
Oxidative Damage ◽  
Plasma Proteins ◽  
Alpha Tocopherol ◽  
Human Blood Plasma ◽  
Lipid Hydroperoxides ◽  
Sh Groups ◽  
Toxic Species

Endothelial cells and activated phagocytes produce both nitric oxide (.NO) and superoxide (O2.-), which react to form peroxynitrite. Peroxynitrite has been suggested to be directly cytotoxic and also to decompose into other toxic species. In order to understand the consequences of peroxynitrite generation in vivo, we examined its reaction with human blood plasma. Peroxynitrite decreased the total peroxyl-trapping capacity of plasma. In terms of specific antioxidants, addition of peroxynitrite to plasma leads to rapid oxidation of ascorbic acid, uric acid and plasma SH groups. The oxidation of plasma SH groups was enhanced in dialysed plasma and returned to control levels by the addition of physiological levels of bicarbonate. Evidence was found for formation of nitro-adducts to aromatic side chains in plasma proteins by peroxynitrite. Peroxynitrite also leads to depletion of ubiquinol and formation of traces of lipid hydroperoxides in plasma, although alpha-tocopherol levels were only slightly decreased. Peroxynitrite formation in human body fluids is likely to cause antioxidant depletion and oxidative damage.

scholarly journals Vitamin E Supplementation and Mitochondria in Experimental and Functional Hyperthyroidism: A Mini-Review

Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2900 ◽  
Author(s):  
Gaetana Napolitano ◽  
Gianluca Fasciolo ◽  
Sergio Di Meo ◽  
Paola Venditti
Keyword(s):  
Vitamin E ◽  
Oxidative Damage ◽  
Cell Function ◽  
Peroxyl Radicals ◽  
Antioxidant Vitamin ◽  
Mitochondrial Ros ◽  
Mitochondrial Population ◽  
Vitamin E Supplementation ◽  
Lipid Soluble Antioxidant

Mitochondria are both the main sites of production and the main target of reactive oxygen species (ROS). This can lead to mitochondrial dysfunction with harmful consequences for the cells and the whole organism, resulting in metabolic and neurodegenerative disorders such as type 2 diabetes, obesity, dementia, and aging. To protect themselves from ROS, mitochondria are equipped with an efficient antioxidant system, which includes low-molecular-mass molecules and enzymes able to scavenge ROS or repair the oxidative damage. In the mitochondrial membranes, a major role is played by the lipid-soluble antioxidant vitamin E, which reacts with the peroxyl radicals faster than the molecules of polyunsaturated fatty acids, and in doing so, protects membranes from excessive oxidative damage. In the present review, we summarize the available data concerning the capacity of vitamin E supplementation to protect mitochondria from oxidative damage in hyperthyroidism, a condition that leads to increased mitochondrial ROS production and oxidative damage. Vitamin E supplementation to hyperthyroid animals limits the thyroid hormone-induced increases in mitochondrial ROS and oxidative damage. Moreover, it prevents the reduction of the high functionality components of the mitochondrial population induced by hyperthyroidism, thus preserving cell function.

scholarly journals l-carnosine (β-alanyl-l-histidine) and carcinine (β-alanylhistamine) act as natural antioxidants with hydroxyl-radical-scavenging and lipid-peroxidase activities

1994 ◽  
Vol 304 (2) ◽  
pp. 509-516 ◽  
Author(s):  
M A Babizhayev ◽  
M C Seguin ◽  
J Gueyne ◽  
R P Evstigneeva ◽  
E A Ageyeva ◽  
...  
Keyword(s):  
Linoleic Acid ◽  
Direct Reduction ◽  
Radical Scavenging ◽  
Thiobarbituric Acid ◽  
Natural Antioxidants ◽  
Peroxyl Radicals ◽  
Lipid Phase ◽  
Oh Radicals ◽  
Thiobarbituric Acid Reactive Substance ◽  
Lipid Hydroperoxides

Carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) are natural imidazole-containing compounds found in the non-protein fraction of mammalian tissues. Carcinine was synthesized by an original procedure and characterized. Both carnosine and carcinine (10-25 mM) are capable of inhibiting the catalysis of linoleic acid and phosphatidylcholine liposomal peroxidation (LPO) by the O2(-.)-dependent iron-ascorbate and lipid-peroxyl-radical-generating linoleic acid 13-monohydroperoxide (LOOH)-activated haemoglobin systems, as measured by thiobarbituric-acid-reactive substance. Carcinine and carnosine are good scavengers of OH. radicals, as detected by iron-dependent radical damage to the sugar deoxyribose. This suggests that carnosine and carcinine are able to scavenge free radicals or donate hydrogen ions. The iodometric, conjugated diene and t.l.c. assessments of lipid hydroperoxides (13-monohydroperoxide linoleic acid and phosphatidylcholine hydroperoxide) showed their efficient reduction and deactivation by carnosine and carcinine (10-25 mM) in the liberated and bound-to-artificial-bilayer states. This suggests that the peroxidase activity exceeded that susceptible to direct reduction with glutathione peroxidase. Imidazole, solutions of beta-alanine, or their mixtures with peptide moieties did not show antioxidant potential. Free L-histidine and especially histamine stimulated iron (II) salt-dependent LPO. Due to the combination of weak metal chelating (abolished by EDTA), OH. and lipid peroxyl radicals scavenging, reducing activities to liberated fatty acid and phospholipid hydroperoxides, carnosine and carcinine appear to be physiological antioxidants able to efficiently protect the lipid phase of biological membranes and aqueous environments.

Theoretical study on the oxidative damage to cholesterol induced by peroxyl radicals

2015 ◽  
Vol 28 (7) ◽  
pp. 504-508 ◽  
Author(s):  
Manuel E. Medina ◽  
Annia Galano ◽  
Ángel Trigos
Keyword(s):  
Oxidative Damage ◽  
Theoretical Study ◽  
Peroxyl Radicals

scholarly journals Comprehensive Evaluation of the Oral Health Status, Salivary Gland Function, and Oxidative Stress in the Saliva of Patients with Subacute Phase of Stroke: A Case-Control Study

2020 ◽  
Vol 9 (7) ◽  
pp. 2252 ◽  
Author(s):  
Piotr Gerreth ◽  
Mateusz Maciejczyk ◽  
Anna Zalewska ◽  
Karolina Gerreth ◽  
Katarzyna Hojan
Keyword(s):  
Salivary Gland ◽  
Health Status ◽  
Oral Health ◽  
Oxidative Damage ◽  
Oral Health Status ◽  
Study Group ◽  
Lipid Hydroperoxides ◽  
Stroke Patients ◽  
Subacute Phase ◽  
Oxidative Damage To Proteins

This is the first study to assess, comprehensively, the oral health status; salivary glands’ function and enzymatic and non-enzymatic antioxidant defense; and oxidative damage to proteins and lipids in the non-stimulated (NWS) and stimulated (SWS) whole saliva of stroke patients. The study included 30 patients in the subacute phase of the stroke and an age and gender-matched control group. We showed that the activity of antioxidant enzymes (catalase and salivary peroxidase) was significantly higher in both NWS and SWS of stroke patients, similarly to uric acid concentration. However, in the study group, the reduced glutathione (GSH) concentration in SWS decreased. The contents of protein glycooxidation products (advanced glycation end products (AGE) and protein oxidation products (AOPP)) and lipid hydroperoxides were significantly higher in NWS and SWS of stroke patients. In the study group there was also a decrease in stimulated saliva secretion and total protein content. Interestingly, products of protein and lipid oxidation correlate negatively with SWS flow. The ROC analysis showed that salivary GSH with 100% specificity and 100% sensitivity differentiates the analyzed groups (AUC = 1.0). To sum up, in subacute stroke patients there are redox imbalances and oxidative damage to proteins and lipids in non-stimulated and stimulated saliva. Stroke patients also suffer from salivary gland dysfunction.

scholarly journals Blood Profile of Cytokines, Chemokines, Growth Factors, and Redox Biomarkers in Response to Different Protocols of Treadmill Running in Rats

2020 ◽  
Vol 21 (21) ◽  
pp. 8071 ◽  
Author(s):  
Elżbieta Supruniuk ◽  
Mateusz Maciejczyk ◽  
Anna Zalewska ◽  
Jan Górski ◽  
Adrian Chabowski
Keyword(s):  
Growth Factors ◽  
Oxidative Damage ◽  
Nitrosative Stress ◽  
Exercise Bout ◽  
Sport Performance ◽  
Treadmill Running ◽  
Lipid Hydroperoxides ◽  
Blood Profile ◽  
Monocyte Chemoattractant Protein 1 ◽  
Inflammatory Status

Both positive and negative aspects of sport performance are currently considered. The aim of our study was to determine time- and intensity-dependent effects of a single exercise bout on redox and inflammatory status. The experiment was performed on 40 male Wistar rats subjected to treadmill running for 30 min with the speed of 18 m/min (M30) or 28 m/min (F30), or for 2 h with the speed of 18 m/min (M120). Immunoenzymatic and spectrophotometric methods were applied to assess the levels of pro-inflammatory and anti-inflammatory cytokines, chemokines, growth factors, the antioxidant barrier, redox status, oxidative damage products, nitrosative stress, and their relationships with plasma non-esterified fatty acids. Treadmill running caused a reduction in the content of monocyte chemoattractant protein-1 (MCP1) and nitric oxide (M30, M120, F30 groups) as well as macrophage inflammatory protein-1α (MIP-1α) and regulated on activation, normal T-cell expressed and secreted (RANTES) (M30, F30 groups). We also demonstrated an increase in catalase activity as well as higher levels of reduced glutathione, advanced oxidation protein products, lipid hydroperoxides, malondialdehyde (M30, M120, F30 groups), and advanced glycation end products (F30 group). The presented findings showed the activation of antioxidative defense in response to increased reactive oxygen species’ production after a single bout of exercise, but it did not prevent oxidative damage of macromolecules.

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