Alteration in the glutathione, glutathione peroxidase, superoxide dismutase and lipid peroxidation by ascorbic acid in the skin of mice exposed to fractionated γ radiation

2003 ◽  
Vol 332 (1-2) ◽  
pp. 111-121 ◽  
Author(s):  
Ganesh Chandra Jagetia ◽  
G.K. Rajanikant ◽  
Shaival K. Rao ◽  
M. Shrinath Baliga
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Γ Radiation

Oxidative stress in the testis of hyperglycemic rabbits treated with repaglinide

2007 ◽  
Vol 2 (4) ◽  
pp. 538-546
Author(s):  
Anna Gumieniczek ◽  
Hanna Hopkała ◽  
Marcin Pruchniak
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Protective Effect ◽  
Protein Carbonyl ◽  
Carbonyl Groups ◽  
Protein Carbonyl Groups ◽  
Diabetic Rabbits

AbstractIn the present study, the induction of oxidative stress was examined in the testis of alloxan-induced diabetic rabbits. In addition, the protective effect of repaglinide, an oral anti-diabetic, at a dose of 1 mg daily was studied after four and eight weeks of the treatment. For these purposes, the levels of superoxide dismutase (Cu,Zn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), glutathione (GSH), ascorbic acid (AA), lipid peroxidation products (LPO) and protein carbonyl groups (PCG) were quantified. Hyperglycemia resulted in significant increases in the antioxidative enzymes, Cu, Zn-SOD, CAT, GSH-Px, and GSSG-R after four and eight weeks, respectively. There was also an increase in GSH level, and a decrease in the level of AA. These effects were accompanied by an elevation in testicular LPO levels and PCG levels. Repaglinide was found to normalize the activity of GSSG-R and levels of GSH and AA, and blunted the increased lipid peroxidation, however no decrease in PCG levels were observed. In conclusion, some oxidative changes provoked in the testis of rabbits by hyperglycemia, were found to be reduced with repaglinide treatment at therapeutic dose.

scholarly journals Effect of Cross-Sex Hormonal Replacement on Antioxidant Enzymes in Rat Retroperitoneal Fat Adipocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Verónica Guarner-Lans ◽  
Alejandra Zúñiga-Muñoz ◽  
Rodrigo Velázquez Espejel ◽  
Alfredo Cabrera-Orefice ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Enzymatic Activities ◽  
Glutathione S Transferase ◽  
Control Groups ◽  
Intact Female ◽  
Hormonal Replacement

We report the effect of cross-sex hormonal replacement on antioxidant enzymes from rat retroperitoneal fat adipocytes. Eight rats of each gender were assigned to each of the following groups: control groups were intact female or male (F and M, resp.). Experimental groups were ovariectomized F (OvxF), castrated M (CasM), OvxF plus testosterone (OvxF + T), and CasM plus estradiol (CasM + E2) groups. After sacrifice, retroperitoneal fat was dissected and processed for histology. Adipocytes were isolated and the following enzymatic activities were determined: Cu-Zn superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GR). Also, glutathione (GSH) and lipid peroxidation (LPO) were measured. In OvxF, retroperitoneal fat increased and adipocytes were enlarged, while in CasM rats a decrease in retroperitoneal fat and small adipocytes are observed. The cross-sex hormonal replacement in F rats was associated with larger adipocytes and a further decreased activity of Cu-Zn SOD, CAT, GPx, GST, GR, and GSH, in addition to an increase in LPO. CasM + E2exhibited the opposite effects showing further activation antioxidant enzymes and decreases in LPO. In conclusion, E2deficiency favors an increase in retroperitoneal fat and large adipocytes. Cross-sex hormonal replacement in F rats aggravates the condition by inhibiting antioxidant enzymes.

scholarly journals Oxidative Stress in Rats After 60 Days of Hypergalactosemia or Hyperglycemia

2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Glutathione Disulfide ◽  
Hepatic Lipid Peroxidation ◽  
Streptozotocin Diabetic Rats

Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosy-lated hemoglobin A1c concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.

scholarly journals Вплив хлориду кадмію на стан антиоксидантної системи у печінці щурів

2013 ◽  
pp. 102-103
Author(s):  
Б. В. Гутий
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Enzyme Activity ◽  
Glutathione Peroxidase ◽  
Antioxidant System ◽  
Cadmium Chloride

Розкрито особливості антиоксидантної системиорганізму щурів за хронічного кадмієвого токсикозу.Встановлено, що хлорид кадмію у токсичній дозісприяє зниженню активності ферментної й нефер-ментної системи антиоксидантного захисту, на щовказує зниження ферментів глутатіонпероксидази,глутатіонредуктази, супероксиддисмутази, катала-зи та відновленого глутатіону у печінці щурів. Ре-зультати досліджень вказують на те, що хронічнийкадмієвий токсикоз призводить до посиленої акти-вації процесів ліпопероксидації. The features of the antioxidant system of rats with chronic cadmium toxicosiare disclosed. It wasresearched that cadmium chloride in toxic doses reduces enzyme activity of antioxidant system, asindicated by the decrease in enzyme glutathione peroxidase, hlutationreduktazy, superoxide dismutase,catalase and restored glutathione in the liver and blood of rats. The results indicate that chroniccadmium toxicosis leads to enhanced activation of lipid peroxidation.

scholarly journals INFLUENCE OF «METISEVIT» ON THE ACTIVITY OF ENZYME AND NONENZYME LINK OF ANTIOXIDANT PROTECTION UNDER THE BULL’S BODY CADMIUM LOADING

2016 ◽  
Vol 18 (2(66)) ◽  
pp. 52-59
Author(s):  
B.V. Gutyj ◽  
Y. Lavryshyn ◽  
V. Binkevych ◽  
O. Binkevych ◽  
О. Paladischuk ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Antioxidant Defense ◽  
Cadmium Stress ◽  
Antioxidant Defense System ◽  
The Body ◽  
Antioxidant Protection ◽  
Young Cattle

The article contains the research results of the effect of cadmium chloride on the indexes of enzyme and nonenzyme systems of  antioxidant defense system in young cattle, such as the activity of catalase, superoxide dismutase, glutathione peroxidase, glutathione levels of vitamins A and E. It is established that feeding calves at a dose of toxicant 0.04 mg / kg activity of catalase, superoxide dismutase, glutathione peroxidase, glutathione levels of vitamins A and E in the blood of experimental animals decreased throughout the experiment. The lowest indicators of antioxidant in the blood of young cattle is set on the twenty -fourth day of the experiment, which is associated with increased activation of lipid peroxidation and the balance between antioxidant system and lipid peroxidation intensity. Given the cadmium load of young cattle it is used a new integrated drug with antioxidant action «Metisevit», which includes metifen, sodium selenite and vitamin E wich is founded as stimulating effects on the activity of antioxidant protection. In particular,it is established probable increase in activity of catalase, superoxide dismutase, glutathione peroxidase, glutathione levels, vitamin A and vitamin E in the blood of young cattle, which has performed cadmium stress. These changes occur through comprehensive action components of the drug «Metisevit» that leads to the normalization of metabolic processes and free radical in the body of the bull. The results of the research indicate antioxidant drug «Metisevit» in the application of its young cattle and the validity of his administration to improve the body's antioxidant status of chronic cadmium toxicosis.

Dietary supplementation with magnesium citrate may improve pancreatic metabolic indices in an alloxan-induced diabetes rat model

10.5219/1375 ◽  
2020 ◽  
Vol 14 ◽  
pp. 836-846
Author(s):  
Olena Shatynska ◽  
Oleksandr Tokarskyy ◽  
Petro Lykhatskyi ◽  
Olha Yaremchuk ◽  
Iryna Bandas ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Fasting Glucose ◽  
Reduced Glutathione ◽  
Pancreatic Tissue ◽  
Magnesium Supplementation ◽  
Metabolism Enzymes ◽  
Peroxidation Index

The purpose of the current study was to evaluate the protective properties of dietary magnesium supplementation on pancreatic tissue of rats with alloxan-induced diabetes mellitus. Twenty-five male Wistar rats were split into five groups (control, diabetes, diabetes with 100 mg Mg daily, diabetes with 250 mg Mg daily, diabetes with 500 mg Mg daily) with feeding supplementation starting on day 1, diabetes induction on day 21, and animal sacrifice on day 30. Fasting glucose in blood serum was measured on days 21, 25, 27, and day 30. Glucose metabolism enzymes, namely, lactate dehydrogenase and glucose-6-phosphate dehydrogenase, were measured in pancreatic tissue upon the sacrifice, as well as lipid peroxidation, antioxidant system protective enzymes (catalase and superoxide dismutase), and glutathione system components (glutathione reductase, glutathione peroxidase, and glutathione reduced). Pearson correlation coefficients showed strong negative correlation between serum glucose (control and diabetic animals) and glucose metabolism enzymes, catalase, superoxide dismutase, glutathione peroxidase in pancreatic tissue (r >-0.9, p <0.05), moderate negative correlation with reduced glutathione (r = -0.79, p <0.05), moderate positive correlation with lipid peroxidation index (r = +0.67, p <0.05), weak correlation with glutathione reductase (r = -0.57, p <0.05). Magnesium supplementation slowed down diabetes onset considering fasting glucose levels in rats (p <0.05), as well as partially restored investigated dehydrogenase levels in the pancreas of rats comparing to diabetes group (p <0.05). The lipid peroxidation index varied between treatments showing the dose-dependent influence of Mg2+. Magnesium supplementation partially restored catalase and superoxide dismutase activities in pancreatic tissue, as well as glutathione peroxidase and reduced glutathione levels (p <0.05), while glutathione reductase levels remained unaffected (p >0.05). The obtained results suggested a model, where magnesium ions may have a possible protective effect on pancreatic tissue against the negative influence of alloxan inside β cells of the pancreas.

scholarly journals Characterization of Oxidative Stress in Various Tissues of Diabetic and Galactose-fed Rats

2001 ◽  
Vol 2 (3) ◽  
pp. 211-216 ◽  
Author(s):  
Robert M. Strother ◽  
Tonya G. Thomas ◽  
Mary Otsyula ◽  
Ruth A. Sanders ◽  
John B. Watkins III
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Rat Model ◽  
Catalase Activity ◽  
Diabetic Rats ◽  
Oxidized Glutathione ◽  
Hepatic Glutathione ◽  
Reduced And Oxidized Glutathione

Rats fed a galactose-rich diet have been used for several years as a model for diabetes to study, particularly in the eye, the effects of excess blood hexoses. This study sought to determine the utility of galactosemia as a model for oxidative stress in extraocular tissues by examining biomarkers of oxidative stress in galactose-fed rats and experimentally-induced diabetic rats. Sprague-Dawley rats were divided into four groups: experimental control; streptozotocin-induced diabetic; insulin-treated diabetic; and galactose-fed. The rats were maintained on these regimens for 30 days, at which point the activities of catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase, as well as levels of lipid peroxidation and reduced and oxidized glutathione were determined in heart, liver, and kidney. This study indicates that while there are some similarities between galactosemic and diabetic rats in these measured indices of oxidative stress (hepatic catalase activity levels and hepatic and renal levels of oxidized glutathione in both diabetic and galactosemic rats were significantly decreased when compared to normal), overall the galactosemic rat model is not closely parallel to the diabetic rat model in extra-ocular tissues. In addition, several effects of diabetes (increased hepatic glutathione peroxidase activity, increased superoxide dismutase activity in kidney and heart, decreased renal and increased cardiac catalase activity) were not mimicked in galactosemic rats, and glutathione concentration in both liver and heart was affected in opposite ways in diabetic rats and galactose- fed rats. Insulin treatment reversed/prevented the activity changes in renal and cardiac superoxide dismutase, renal and cardiac catalase, and hepatic glutathione peroxidase as well as the hepatic changes in lipid peroxidation and reduced and oxidized glutathione, and the increase in cardiac glutathione. Thus, prudence should be exercised in the use of experimentally galactosemic rats as a model for diabetes until the correspondence of the models has been more fully characterized.

Control of superoxide dismutase, catalase and glutathione peroxidase activities in rat lymphoid organs by thyroid hormones

1994 ◽  
Vol 140 (1) ◽  
pp. 73-77 ◽  
Author(s):  
B Pereira ◽  
L F B P Costa Rosa ◽  
D A Safi ◽  
E J H Bechara ◽  
R Curi
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Thyroid Hormones ◽  
Citrate Synthase ◽  
Lipid Peroxide ◽  
Lymphoid Organs ◽  
Mesenteric Lymph Nodes ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Reducing Equivalents

Abstract This study examined the effect of experimental hyperand hypothyroidism on the superoxide dismutase, catalase and glutathione peroxidase activities of rat lymphoid organs (mesenteric lymph nodes, spleen and thymus) and muscles (soleus and gastrocnemius-white portion) for comparison. The capacity for the generation of reducing equivalents was also investigated: activities of glucose-6-phosphate dehydrogenase (pentose-phosphate pathway) and citrate synthase (Krebs cycle). Hyperthyroidism tended to enhance lipid peroxide content in all tissues. This effect may result from (1) a high capacity for the generation of reducing equivalents in cytosol and mitochondria and (2) a reduced activity of catalase in the lymphoid organs and of glutathione peroxidase in the muscles. The process of lipid peroxidation in these tissues caused by hyperthyroidism was probably slowed down by the augmentation of CuZn- and Mn-superoxide dismutase (Mn-SOD) activities observed under this condition. Hypothyroidism tended to diminish lipid peroxidation and did not affect citrate synthase and glucose-6-phosphate dehydrogenase activities in the lymphoid organs and muscles. Low levels of thyroid hormones tended to diminish Mn-SOD and glutathione peroxidase activities. These findings show that the thyroid hormones might be able to regulate the activities of CuZn- and Mn-SOD, and catalase and glutathione peroxidase in the lymphoid organs and skeletal muscles. Journal of Endocrinology (1994) 140, 73–77

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