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 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 Oxidation of DNA bases, deoxyribonucleosides and homopolymers by peroxyl radicals

1998 ◽  
Vol 335 (2) ◽  
pp. 233-240 ◽  
Author(s):  
Tiberiu SIMANDAN ◽  
Jing SUN ◽  
Thomas A. DIX
Keyword(s):  
Oxidative Damage ◽  
Cellular Systems ◽  
Peroxyl Radicals ◽  
Dna Bases ◽  
Molecular Probe ◽  
Mutagenic Potential ◽  
Dna Base ◽  
Disease Initiation ◽  
Cellular Dna ◽  
In Cells

DNA base oxidation is considered to be a key event associated with disease initiation and progression in humans. Peroxyl radicals (ROO•) are important oxidants found in cells whose ability to react with the DNA bases has not been characterized extensively. In this paper, the products resulting from ROO• oxidation of the DNA bases are determined by gas chromatography/MS in comparison with authentic standards. ROO• radicals oxidize adenine and guanine to their 8-hydroxy derivatives, which are considered biomarkers of hydroxyl radical (HO•) oxidations in cells. ROO• radicals also oxidize adenine to its hydroxylamine, a previously unidentified product. ROO• radicals oxidize cytosine and thymine to the monohydroxy and dihydroxy derivatives that are formed by oxidative damage in cells. Identical ROO• oxidation profiles are observed for each base when exposed as deoxyribonucleosides, monohomopolymers and base-paired dihomopolymers. These results have significance for the development, utilization and interpretation of DNA base-derived biomarkers of oxidative damage associated with disease initiation and propagation, and support the idea that the mutagenic potential of N-oxidized bases, when generated in cellular DNA, will require careful evaluation. Adenine hydroxylamine is proposed as a specific molecular probe for the activity of ROO• in cellular systems.

Oxidative Damage to a Supercoiled DNA by Water Soluble Peroxyl Radicals Characterized with DNA Repair Enzymes

2003 ◽  
Vol 16 (9) ◽  
pp. 1118-1123 ◽  
Author(s):  
Cristina Sanchez ◽  
R. Adam Shane ◽  
Thomas Paul ◽  
Keith U. Ingold
Keyword(s):  
Dna Repair ◽  
Oxidative Damage ◽  
Water Soluble ◽  
Peroxyl Radicals ◽  
Supercoiled Dna ◽  
Dna Repair Enzymes ◽  
Repair Enzymes

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.

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