Intensity of myocardial free-radical processes and expression of glutathione peroxidase and glutathione reductase genes in rats with adrenaline myocarditis

2011 ◽  
Vol 5 (4) ◽  
pp. 357-362
Author(s):  
I. Yu. Iskusnykh ◽  
T. N. Popova ◽  
O. S. Musharova
Keyword(s):  
Free Radical ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Free Radical Processes ◽  
Radical Processes

scholarly journals Expression of Glutathione Peroxidase and Glutathione Reductase and Level of Free Radical Processes under Toxic Hepatitis in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Igor Y. Iskusnykh ◽  
Tatyana N. Popova ◽  
Aleksander A. Agarkov ◽  
Miguel Â. A. Pinheiro de Carvalho ◽  
Stanislav G. Rjevskiy
Keyword(s):  
Free Radical ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Toxic Hepatitis ◽  
Free Radical Oxidation ◽  
Inflammatory Cells ◽  
Maximum Increase ◽  
Radical Oxidation ◽  
Free Radical Processes ◽  
Radical Processes

Correlation between intensity of free radical processes estimated by biochemiluminesce parameters, content of lipoperoxidation products, and changes of glutathione peroxidase (GP, EC 1.11.1.9) and glutathione reductase (GR, EC 1.6.4.2) activities at rats liver injury, after 12, 36, 70, 96, 110, and 125 hours & tetrachloromethane administration have been investigated. The histological examination of the liver sections of rats showed that prominent hepatocytes with marked vacuolisation and inflammatory cells which were arranged around the necrotic tissue are more at 96 h after exposure to CCl4. Moreover maximum increase in GR and GP activities, 2.1 and 2.5 times, respectively, was observed at 96 h after exposure to CCl4, what coincided with the maximum of free radical oxidation processes. Using a combination of reverse transcription and real-time polymerase chain reaction, expression of the glutathione peroxidase and glutathione reductase genes (Gpx1 and Gsr) was analyzed by the determination of their respective mRNAs in the rat liver tissue under toxic hepatitis conditions. The analyses of Gpx1 and Gsr expression revealed that the transcript levels increased in 2.5- and 3.0-folds, respectively. Western blot analysis revealed that the amounts of hepatic Gpx1 and Gsr proteins increased considerably after CCl4administration. It can be proposed that the overexpression of these enzymes could be a mechanism of enhancement of hepatocytes tolerance to oxidative stress.

scholarly journals Intensity of cardiac free-radicals processes and expression of glutathione peroxidase and glutathione reductase genes in rats with adrenaline

2012 ◽  
Vol 58 (5) ◽  
pp. 530-538 ◽  
Author(s):  
I.Y. Iskusnykh ◽  
T.N. Popova ◽  
O.S. Musharova
Keyword(s):  
Free Radical ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Free Radical Oxidation ◽  
Pathological Process ◽  
Mrna Levels ◽  
Maximal Increase ◽  
Radical Oxidation ◽  
Polymerase Chain ◽  
Radical Processes

The correlation between changes in activities of glutathione peroxidase and glutathione reductase in heart of rats during development of adrenaline myocarditis and intensity of free radical processes estimated by biochemiluminesce parameters and the content of lipoperoxidation products was demonstrated. The maximal increase of glutathione peroxidase and glutathione reductase activities (in 1.8 and 1.4 times accordingly) was observed t 24 h after the development of the pathological process; this coincided with the maximum intensity of prosesses of free radical oxidation. Using combination of reverse transcriptions with real-time polymerase chain reaction the cardiac mRNA levels of glutathione peroxidase and glutathione reductase genes were determined during the development of adrenaline myocarditis in rats. Analysis of expression of glutathione peroxidase and glutathione reductase genes showed, that the level of this transcripts demonstrated 2,8- and 7,3- increase in rats with adrenaline myocarditis, respectively. Obviously, overexpression of these enzymes can increase the resistance of cardiomyocites to oxidative stress.

Adaptogenic correction of free radical brain damage in subchronic exposure to sodium fl uoride

2020 ◽  
pp. 381-386
Author(s):  
A. G. Zhukova ◽  
L. G. Gorokhova ◽  
A. S. Kazitskaya ◽  
T. K. Yadykina ◽  
N. N. Mikhailova ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Free Radical ◽  
Brain Tissue ◽  
Free Radical Oxidation ◽  
Radical Oxidation ◽  
Free Radical Processes ◽  
Subchronic Exposure ◽  
Antioxidant Defense Enzymes ◽  
Radical Processes ◽  
Complex Drug

Introduction. Fluorine compounds in small doses, but with prolonged exposure, cause various disorders in organs at the cellular and molecular levels. Activation of free-radical processes plays an important role in the damaging eff ect of fl uorides. Th erefore, one of the most eff ective ways to limit fl uorine-induced damage is to directly aff ect free-radical processes using herbal preparations with antioxidant properties.The aim of the study is to study the eff ect of a dihydroquercetin-based drug on the activity of free radical processes in brain tissue under subchronic exposure to sodium fl uoride (NaF).Materials and methods. Th e work was performed on white male laboratory rats weighing 200-250 g. Th e rats were divided into 3 groups: 1 — control; 2 — rats with chronic exposure to sodium fl uoride (NaF) for 9 weeks; 3 — rats receiving a NAF solution with simultaneous administration of a complex drug based on dihydroquercetin at a dose of 3 mg/kg in 1% starch gel for 3, 6 and 9 weeks. The activity of free radical oxidation and antioxidant defense enzymes — superoxide dismutase (SOD) and catalase-was determined in the cerebral cortex. Th e level of expression of hypoxia-induced transcription factor HIF — 1A and inducible forms of proteins HSP72 and HSP32 were determined in the cytosolic fraction of brain tissue.Results. In the early stages of subchronic fl uoride exposure (1-3 weeks), the expression of protective proteins HIF-1α, HSP72, HSP32 and catalase was shown in the rat cortex, as a result of which the activity of free-radical processes was maintained at the control level. An increase in the timing of fl uoride intake to 9 weeks led to a decrease in antioxidant protection and signifi cant activation of free radical oxidation in brain tissue. Daily administration of a complex drug with dihydroquercetin for 3, 6 and 9 weeks to rats with subchronic fl uoride exposure led to a decrease in the severity of pro- and antioxidant balance disorders in the cerebral cortex. At the same time, the greatest protective eff ect of dihydroquercetin with fl uoride exposure was manifested by the 9th week of its administration.Conclusions. When subchronic intake of fl uorides in the body, the drug based on dihydroquercetin has a neuroprotective eff ect, which is manifested by an increase in the activity of antioxidant enzymes of fr ee radical oxidation and catalase and the resistance of the cortex to induced fr ee radical oxidation.

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