The Peroxidase Activity of a Hemin−DNA Oligonucleotide Complex:  Free Radical Damage to Specific Guanine Bases of the DNA†

2001 ◽  
Vol 123 (7) ◽  
pp. 1337-1348 ◽  
Author(s):  
Paola Travascio ◽  
Paul K. Witting ◽  
A. Grant Mauk ◽  
Dipankar Sen
Keyword(s):  
Free Radical ◽  
Peroxidase Activity ◽  
Free Radical Damage ◽  
Radical Damage

Study of antioxidant potential in leaves, stems, nuts of Juglans regia L.

2012 ◽  
Vol 1 (10) ◽  
pp. 79 ◽  
Author(s):  
G. Raja* ◽  
Ivvala Anand Shaker ◽  
Inampudi Sailaja ◽  
R. Swaminathan ◽  
S. Saleem Basha ◽  
...  
Keyword(s):  
Free Radicals ◽  
Free Radical ◽  
Antioxidant Activities ◽  
Radical Scavenging Activity ◽  
Juglans Regia ◽  
Radical Scavenging ◽  
Antioxidant Compounds ◽  
Free Radical Damage ◽  
Radical Damage

Natural antioxidants can protect the human body from free radicals and retard the progress of many chronic diseases as well as lipid oxidative rancidity in foods. The role of antioxidants has protected effect against free radical damage that may cause many diseases including cancer. Primary sources of naturally occurring antioxidants are known as whole grains, fruits, and vegetables. Several studies suggest that regular consumption of nuts, mostly walnuts, may have beneficial effects against oxidative stress mediated diseases such as cardiovascular disease and cancer. The role of antioxidants has attracted much interest with respect to their protective effect against free radical damage that may cause many diseases including cancer. Juglans regia L. (walnut) contains antioxidant compounds, which are thought to contribute to their biological properties. Polyphenols, flavonoids and flavonols concentrations and antioxidant activity of Leaves, Stems and Nuts extract of Juglans regia L. as evaluated using DPPH, ABTS, Nitric acid, hydroxyl and superoxide radical scavenging activity, lipid peroxidation and total oxidation activity were determined. The antioxidant activities of Leaves, Stems and Nuts extract of Juglans regia L. were concentration dependent in different experimental models and it was observed that free radicals were scavenged by the test compounds in all the models.

Cyclical estrogen and free radical damage to the rabbit urinary bladder

2009 ◽  
Vol 21 (4) ◽  
pp. 489-494 ◽  
Author(s):  
Alexandra Rehfuss ◽  
Catherine Schuler ◽  
Christina Maxemous ◽  
Robert E. Leggett ◽  
Robert M. Levin
Keyword(s):  
Free Radical ◽  
Urinary Bladder ◽  
Free Radical Damage ◽  
Radical Damage ◽  
Rabbit Urinary Bladder

Iron overload, free radical damage, and rhesus haemolytic disease

The Lancet ◽  
1990 ◽  
Vol 335 (8695) ◽  
pp. 933-936 ◽  
Author(s):  
H.M. Berger ◽  
J.H.N. Lindeman ◽  
D. van Zoeren-Grobben ◽  
E. Hudkamp ◽  
H.H. Kanhai ◽  
...  
Keyword(s):  
Free Radical ◽  
Iron Overload ◽  
Free Radical Damage ◽  
Haemolytic Disease ◽  
Radical Damage

scholarly journals Acidosis-Induced Ischemic Brain Damage: Are Free Radicals Involved?

1991 ◽  
Vol 11 (4) ◽  
pp. 587-596 ◽  
Author(s):  
Johan Lundgren ◽  
Hui Zhang ◽  
Carl-David Agardh ◽  
Maj-Lis Smith ◽  
Patrica J. Evans ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Free Radical ◽  
Substantia Nigra ◽  
Brain Damage ◽  
Oxygen Species ◽  
Total Glutathione ◽  
Free Radical Damage ◽  
Free Iron ◽  
Radical Damage

Substantial evidence exists that reactive oxygen species participate in the pathogenesis of brain damage following both sustained and transient cerebral ischemia, adversely affecting the vascular endothelium and contributing to the formation of edema. One likely triggering event for free radical damage is derealization of protein-bound iron. The binding capacity for some iron-binding proteins is highly pH sensitive and, consequently, the release of iron is enhanced by acidosis. In this study, we explored whether enhanced acidosis during ischemia triggers the production of reactive oxygen species. To that end, enhanced acidosis was produced by inducing ischemia in hyperglycemic rats, with normoglycemic ones serving as controls. Production of H2O2, estimated from the decrease in catalase activity after 3-amino-1,2,4-triazole (AT) administration, was measured in the cerebral cortex, caudoputamen, hippocampus, and substantia nigra (SN) after 15 min of ischemia followed by 5, 15, and 45 min of recovery, respectively (in substantia nigra after 45 min of recovery only). Free iron in cerebrospinal fluid (CSF) was measured after ischemia and 45 min of recovery. Levels of total glutathione (GSH + GSSH) in cortex and hippocampus, and levels of α-tocopherol in cortex, were also measured after 15 min of ischemia followed by 5, 15, and 45 min of recovery. The results confirm previous findings that brief ischemia in normoglycemic animals does not measurably increase H2O2 production in AT-injected animals. Ischemia under hyperglycemic conditions likewise failed to induce increased H2O2 production. No difference in free iron in CSF was observed between animals subjected to ischemia under hyper- and normoglycemic conditions. The moderate decrease in total glutathione or α-tocopherol levels did not differ between normo- and hyperglycemic animals in any brain region or at any recovery time. Thus, the results failed to give positive evidence for free radical damage following brief periods of ischemia complicated by excessive acidosis. However, it is possible that free radical production is localized to a small subcellular compartment within the tissue, thereby escaping detection. Also, the results do not exclude the possibility that free radicals are pathogenetically important after ischemia of longer duration.

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