scholarly journals Immunolocalization of Glutathione-Peroxidase (GPx1) in the Rat Adrenal Cortex: Correlation between Steroidogenesis and Lipid Peroxidation

2017 ◽  
Vol 50 (2) ◽  
pp. 57-61 ◽  
Author(s):  
Masanori Murakoshi ◽  
Robert Yoshiyuki Osamura
2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Verónica Guarner-Lans ◽  
Alejandra Zúñiga-Muñoz ◽  
Rodrigo Velázquez Espejel ◽  
Alfredo Cabrera-Orefice ◽  
...  

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.


2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins

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.


2020 ◽  
Vol 174 (2) ◽  
pp. 80-85
Author(s):  
R. G. Myazin ◽  
D. N. Emel’yanov

The aim of this study was to study the eff ects of using the infusion drug Remaxol in young patients with alcoholic liver disease.Materials and methods: the clinical and laboratory data of 80 young patients with alcoholic liver disease were analyzed, divided depending on the treatment regimen into 2 groups: the main (n = 44) who received Remaxol according to the scheme: 400 ml iv, drip, at a rate 40–60 drops per minute daily, course No. 5–10, and control (n = 36) — received basic therapy. In all patients, the dynamics in blood serum was studied: lipid peroxidation indices (malondialdehyde, diene conjugates), antioxidant protection enzymes (catalase, SOD, glutathione peroxidase), markers of cytolysis, cholestasis and lipid metabolism.Results: initially there was a significant increase in lipid peroxidation processes, accompanied by slight stimulation of the antioxidant system of the liver and pronounced signs of cytolysis and cholestasis. The inclusion of Remaxol in treatment regimens leads to a significant decrease in the level of malondialdehyde and diene conjugates, and the restoration of the antioxidant system (increase in catalase, SOD, and glutathione peroxidase). At the same time, a marked decrease in the syndromes of cytolysis and cholestasis was noted, which was accompanied by an improvement in the condition of the patients: cessation of nausea, restoration of appetite and sleep, and improvement of well-being.


Author(s):  
Б. В. Гутий

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.


2016 ◽  
Vol 18 (2(66)) ◽  
pp. 52-59
Author(s):  
B.V. Gutyj ◽  
Y. Lavryshyn ◽  
V. Binkevych ◽  
O. Binkevych ◽  
О. Paladischuk ◽  
...  

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.


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