Lipid Peroxidation and Glutathione Peroxidase, Glutathione Reductase, Superoxide Dismutase, Catalase, and Glucose-6-Phosphate Dehydrogenase Activities in FeCl3-Induced Epileptogenic Foci in the Rat Brain

Epilepsia ◽  
1990 ◽  
Vol 31 (1) ◽  
pp. 15-26 ◽  
Author(s):  
Rameshwar Singh ◽  
Deena Nath Pathak
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.


10.5219/1375 ◽  
2020 ◽  
Vol 14 ◽  
pp. 836-846
Author(s):  
Olena Shatynska ◽  
Oleksandr Tokarskyy ◽  
Petro Lykhatskyi ◽  
Olha Yaremchuk ◽  
Iryna Bandas ◽  
...  

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.


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

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


2019 ◽  
Vol 0 (0) ◽  
Author(s):  
Varsha Shukla ◽  
Siddharth Kumar Das ◽  
Abbas Ali Mahdi ◽  
Shweta Agarwal ◽  
Sukhanshi Khandpur

Summary Background Fibromyalgia syndrome (FMS) is characterized by altered pain perception with chronic, widespread musculoskeletal pain. The relationship between nitric oxide, oxidative stress and the severity of FMS has not been studied. This study evaluated NO levels in plasma, LPO products and antioxidants in Red Cell lysate in patients of FMS and correlated it with disease severity. Methods 105 FMS patients who fulfilled 1990 ACR Criteria and 105 age- and sex-matched healthy controls were recruited over two years from 2013 to 2015. Antioxidative enzyme activity was assessed by the estimation of catalase, glutathione peroxidase (GPx) and glutathione reductase (GR) and superoxide dismutase (SOD). Nitric oxide in plasma, MDA marker of lipid peroxidation (LPO) in the lysate was donen for estimating oxidative stress. FIQR was used to assess the severity of fibromyalgia. Results The catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase levels were significantly low in patients than controls (p<0.001). Plasma NO levels and LPO were also significantly high (p<0.05). NO and LPO levels showed a significant positive correlation with FIQR (r: 0.57, 0.8 and p: <0.001) whereas a negative correlation was observed between antioxidants (Cat, GR and GPx, but not SOD) and FIQR. Conclusions Low antioxidants and raised LPO in RBC lysate in patients with FM together with high plasma NO correlated with the severity of FMS.


2001 ◽  
Vol 47 (11) ◽  
pp. 987-993 ◽  
Author(s):  
Varinder K Randhawa ◽  
Fengzhen Zhou ◽  
Xiaolei Jin ◽  
Czesia Nalewajko ◽  
Donn J Kushner

Treatment with Ni(NO3)2 leads to the formation of reactive oxygen species (ROS) in the green alga Scenedesmus acutus f. alternans, causing lipid peroxidation. This effect was stronger in a Ni-sensitive strain, UTEX72, than in a Ni-resistant strain, B4. In the resistant strain, Ni induced an increased ratio of reduced to oxidized glutathione (GSH:GSSG), whereas it caused a lowered ratio in the sensitive strain. Enzymes involved in the control of ROS were studied in these strains as well as two others that have shown different degrees of nickel resistance. The resistant strain, B4, which grows while containing large amounts of internal Ni, had much higher levels of glutathione reductase and catalase than the other strains. The sensitive strain, UTEX72, had higher levels of glutathione peroxidase, superoxide dismutase, and glucose-6-phosphate dehydrogenase than did strain B4. The resistant strains, Ni-Tol and Cu-Tol, derived from strain UTEX72, which are partly able to exclude Ni, had enzyme profiles that resembled that of UTEX72 more closely than that of B4. Treatment with 10 and 100 µM Ni for 4 or 22 h had complex effects on enzyme levels in all four strains. Ni decreased glutathione reductase in B4, slightly increased it in Ni-Tol and Cu-Tol, and did not affect the low levels of this enzyme in UTEX72. Ni lowered glutathione peroxidase in B4 and either did not affect it or slightly raised it in the other strains. Ni lowered catalase in B4 and did not affect the other strains. Superoxide dismutase was raised in B4 and Ni-Tol and lowered in Cu-Tol and UTEX72, and glucose-6-phosphate dehydrogenase was lowered in all four strains. These results suggest that one major mechanism of Ni resistance, especially in strain B4, may be the ability to combat the formation of ROS when exposed to this metal, likely by maintaining a high GSH:GSSG ratio.Key words: Scenedesmus acutus f. alternans, glutathione reductase, glutathione peroxidase, catalase, superoxide dismutase, glucose-6-phosphate dehydrogenase, lipid peroxidation, nickel, reactive oxygen species.


2010 ◽  
Vol 56 (5) ◽  
pp. 596-601 ◽  
Author(s):  
V.V. Kostyushov ◽  
I.I. Bokal ◽  
S.A. Petrov

HIV infection is accompanied by activation of lipid peroxidation, oxidative modification of lipoprotein complexes, and a decrease in activity of antioxidant enzymes (superoxide dismutase (SOD), catalase and glutathione peroxidase (GP)) in blood serum. A significant increase of glutathione reductase observed under these conditions is considered as a function of the antioxidant defence. These changes were already seen at early (symptomless) stages of this disease, however, at manifested forms they were more pronounced.


The indicators of the activity of lipid peroxidation and the antioxidant system were studied in dynamics in 158 patients with infectious mononucleosis depending on the severity of the clinical course of the disease. It is proved that lipid peroxidation is significantly activated in patients with infectious mononucleosis as the severity of the disease increases and therefore increases the oxidative activity of blood plasma, the concentration of dyne conjugates and malondialdehyde in the blood, decreases the activity of antioxidant enzymes of erythrocytes (catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase), glutathione peroxidase and glutathione reductase activity in plasma and lowering the concentration of total and reduced glutathione in the blood, as well as reduce the antioxidant activity of blood plasma and erythrocytes. Lipid peroxidation significantly increase and the activity of the antioxidant system decrease in patients with infectious mononucleosis in the acute period of the disease, as evidenced by the increased concentration of dyne conjugates, malonic dialdehyde and total oxidative plasma activity in the blood, reduced activity of the total antioxidant activity of plasma and erythrocytes, the decrease in the activity of antioxidant enzymes of erythrocytes catalase, superoxide dismutase, glutathione peroxidase, glutathione peroxidase and glutathione reductase of blood plasma, the decrease in the concentration of glutathione in the blood. The most pronounced disorders of lipid peroxidation and antioxidant system activity were found in patients with moderate-severe and severe infectious mononucleosis. The development of cytolytic syndrome in infectious mononucleosis is associated with the action of reactive oxygen forms species and lipid hydroperoxide.


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.


1982 ◽  
Vol 204 (2) ◽  
pp. 535-540 ◽  
Author(s):  
I Mavelli ◽  
A Rigo ◽  
R Federico ◽  
M R Ciriolo ◽  
G Rotilio

The specific activities of Cu, Zn- and Mn-superoxide dismutases, of glutathione peroxidase and of catalase, the enzymes considered to be specifically involved in the defence of the cell against the partially reduced forms of oxygen, were determined as the function of postnatal age in the early (up to 60 days) period of rat brain development. The enzymes were assayed in the cytoplasmic fraction, in the crude mitochondrial fraction including peroxisomes, and in the mitochondria. The results show that the temporal changes of these enzymes cannot be correlated with each other, thus indicating that they do not concertedly parallel the increasing activity of aerobic brain metabolism during development. Specifically the cytoplasmic fraction shows a gradual increase of the Cu, Zn-superoxide dismutase activity with age, whereas the glutathione peroxidase activity is constant from birth. Furthermore the increase of the mitochondrial Mn-superoxide dismutase as a function of postnatal age is more remarkable than that of the cytoplasmic Cu, Zn-enzyme. Higher activities of catalase in adult animals are detectable only in the subcellular fraction containing peroxisomes, because of the modest catalase activity of the brain. These results indicate independent regulation of the expression of these enzyme activities in the process of brain differentiation and point to a relative deficiency of enzymic protection of the brain differentiation and point to a relative deficiency of enzymic protection of the brain against potentially toxic oxygen derivatives. This situation is similar to the pattern already described in the rat heart and in rat and mouse ascites-tumour cells, at variance with the much more efficient enzyme pattern present in rat hepatocytes.


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