Glutathione Peroxidase Activity In Rats Research Articles

Effects of Combined Hypothyroidism and Selenium Deficiency on Selenoenzyme Glutathione Peroxidase Activity in Rats

Abstract The effects of propylthiouracil (PTU) treatment and selenium-deficient diet on selenium and thyroid status of Wistar male rats were examined in this study. Wistar male rats (n =128) were divided into four groups: (1) control group – selenium-adequate rats fed a diet supplemented with 0.334 mg Na selenite/kg feed and received regular drinking water (Se+PTU-); (2) selenium adequate rats fed a diet supplemented with 0.334 mg Na selenite/kg feed and received a dose of 150 mg/L of PTU in drinking water, (Se+PTU+); (3) selenium-deficient rats fed a diet containing 0.031 mg Na selenite/ kg and received regular drinking water (Se-PTU-); (4) selenium deficient rats fed a diet containing 0.031 mg Na selenite/kg and received 150 mg/L of PTU in drinking water (Se-PTU+). After three and seven weeks of treatment, all Se – animals had significantly lower whole blood Se concentrations and GPx1 and GPx3 activities. PTU induced a significant decrease in T4 and T3 plasma concentrations after three weeks of treatment in both PTU+ groups. Furthermore, after seven weeks, the T3 level was close to its detection limit in Se – animals. A negative correlation was spotted between GPx activity and concentration of T3 after three and seven weeks. It could indicate an inhibitory influence of thyroid hormones on the expression and/or activities of GPx enzymes related to the available Se in conditions of systemic decrease of T4 concentration. This effect was particularly pronounced in Se – animals.

Curcumin Enhanced the Neomucosa Formation by Mediating the Antioxidation Mechanism in Rats.

Objectives:The purpose of the study was to examine the possible effects of curcumin on the formation of neomucosa in parietal peritoneum which was applied as a patch for terminal ileal defect in rats.Methods:Sixteen male Wistar Hannover rats were split into two groups. The control group was injected with saline and curcumin (2 mL/kg/day, by gavage) was given to the experimental group. In both groups, amounts of 8-hydroxy-2’-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), the activities of glutathione peroxidase and superoxide dismutase were determined in serum. The development of neomucosa formation was examined morphologically.Results:Serum antioxidant levels and glutathione peroxidase activity in rats given curcumin were significantly higher than those of the control group (p<0.05). The levels of oxidative markers (MDA and 8-OHdG) in rats given curcumin were significantly lower than those of the control group (p<0.05). In the histopathological examination, 62.5% of rats in the curcumin group showed formation of neomucosa while 37.5% of control rats showed neomucosa.Conclusion:The use of curcumin in rats with terminal ileal defect enhanced the formation of neomucosa by decreasing the oxidation level and increasing the antioxidation level. Curcumin may be used in the patients with short bowel syndrome to increase the absorption surface area.

Evaluation of oxaliplatin-induced pulmonary toxicity in rats.

IntroductionThe mechanism of oxaliplatin (OXA) induced pulmonary toxicity is not fully understood.Aim of the studyThe present study was designed to investigate the pulmonary toxicity of OXA that has been reported in previous studies. Study design: animal experiments.Material and methodsA total of 40 female Wistar rats were divided into 5 groups. In group 1, 5% glucose was injected intra-peritoneally; then the rats were sacrificed on day 14. OXA was administered in groups 2, 3, 4, and 5; then the animals were sacrificed on day 7 in group 2, day 14 in group 3, day 28 in group 4 and day 48 in group 5. The groups were further categorized as short-term administration and long-term administration groups. Furthermore, tissue glutathione peroxidase (GPX) activity was measured in all rats.ResultsThe mean GPX activities were 0.66 U/mg in the sham group, 0.74 U/mg in the short-term groups, and 0.74 U/mg in the long-term groups. We found that long-term OXA administration causes pulmonary toxicity resulting in increased intra-alveolar/interstitial macrophages and interstitial pneumonia. Similarly, we found reduced and permanent tissue GPX activity in rats that received OXA in higher doses and for a long term.ConclusionsLong-term OXA therapy causes toxic changes in the lung tissue.

The protective effects of taurine on experimental acute pancreatitis in a rat model

The aim of this study was to investigate the protective effects of taurine (Tau) on experimental acute pancreatitis (AP) in a rat model by measuring cytokines and oxidant stress markers. Forty rats were randomly divided into four groups: sham, AP, Tau and AP + Tau. AP was induced with sodium taurocholate. No treatment was given to the AP. All rats were killed 5 days later. Pancreatic tissues of rats and blood samples were obtained. Tau treatment significantly decreased serum amylase activity (p < 0.001), total injury score (p < 0.001), malondialdehyde levels (p < 0.001) and myeloperoxidase (MPO) activity (p < 0.001). There was no significant difference between the Tau and AP + Tau groups in serum and pancreatic tumor necrosis factor-α, interleukin (IL)-1β and IL-6 levels (p = 1.000). Histopathologic scores in the AP + Tau and Tau groups were significantly lower compared with the AP group (both p < 0.001). These results showed that Tau reduces lipid peroxidation, amylase and MPO activities and the concentrations of proinflammatory cytokines secondary to AP and also increases superoxide dismutase and glutathione peroxidase activities in rats with sodium taurocholate-induced AP. It also has a marked ameliorative effect at histopathologic lesions. With these effects, Tau protects the cells from oxidative damage, reduces inflammation and promotes regression of pancreatic damage.

결명자 추출물이 D-Galactosamine 유발 간 손상에 미치는 영향

This study was performed to evaluate the biological activity and protective effect of Cassia tora ethanol extracts against D-galactosamine induced hepatotoxicity in rats. Male Sprague-Dawley rats were grouped into normal group, D-galactosamine treated group(control), D-galactosamine plus 0.25% Cassia tora extracts treated group and D-galactosamine plus 0.5% Cassia tora extracts treated group. Normal and control group were fed control diet and Cassia tora extracts treated groups were fed experimental diets containing 0.25% or 0.5% Cassia tora ethanol extracts for 5 weeks. Body weight gain and liver weight of rats were not significantly different between groups. Cholesterol and triglyceride concentrations in serum and liver were significantly lower in rats treated only with D-galactosamine compared to normal group, and improved in Cassia tora extracts supplemented rats. D-galactosamine treatment significantly increased serum aspartate transaminase, alanine transaminase, gamma glutamyl transferase and alkaline phosphatase, however, the activities of aspartate transaminase and alanine transaminase were significantly decreased in Cassia tora extracts supplemented rats when compared with D-galactosamine treated control group. Cassia tora extracts significantly suppressed the D-galactosamine-induced elevation of liver thiobarbituric acid reactive substances(TBARS) contents. Superoxide dismutase activity was decreased by D-galactosamine treatment, however by the supplementation of Cassia tora ethanol extracts, significantly increased in dose-dependent manner. Glutathione peroxidase activity in rats fed diets containing Cassia tora extracts was decreased compared to control. Based on these results, we concluded that Cassia tora ethanol extracts may prevents the D-galactosamine-induced hepatotoxicity probably via an antioxidant mechanism.

Temporal and regional changes of superoxide dismutase and glutathione peroxidase activities in rats exposed to focal cerebral ischemia

Reactive oxygen species are important cause of tissue injury during cerebral ischemia and reperfusion (I/R). Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) are intracellular enzymes responsible for endogenous antioxidant defense of tissues affected by I/R. The aim of this study was to examine temporal and regional changes of SOD and GSH-Px activities in animals exposed to transient focal cerebral ischemia. Male Wistar Hannover rats were subjected to the right middle cerebral artery occlusion for 2 h. The animals were sacrificed immediately, 0·5, 1, 2, 3, 6, 24, 48, 72 or 168 h after ischemic procedure. SOD and GSH-Px activities were determined spectrophotometrically in the hippocampus and parietal cortex, both unilaterally and contralaterally to the occlusion. Sham-operated animals were used as the control group. Our results indicated that transient focal cerebral ischemia causes significant changes in SOD activities in the hippocampus and parietal cortex such as in GSH-Px activities in the parietal cortex, unilaterally and contralaterally to the lesion in rats during different reperfusion periods. Statistically significant activation of GSH-Px was registered neither in the right nor in the left hippocampus of ischemic animals.

Pineal gland glutathione peroxidase activity in rats and its age-associated change

The glutathione peroxidase activity in the pineal gland (epiphysis) has been studied in young and aging Wistar female rats (2–4 and 17–19 months old). For comparison, the same activity was studied in the pyramids of the medulla oblongata and in the olfactory tubercle. These two brain structures represent white and gray matter, respectively. The activity was evaluated using H2O2 as a redox substrate and with 5,5′-dithiobis-(2-nitrobenzoic acid) to determine the decline in the level of the reduced glutathione. The glutathione peroxidase activity was higher in the pineal gland than in the brain structures studied. Pineal glutathione peroxidase activities (micromole of GSH per minute per milligram of protein, M ± m) in young and old rats were 1.52 ± 0.07 and 1.27 ± 0.06, respectively (p < 0.05). The decline in enzymatic activity found in the aged rats could be due to an age-associated decrease in selenium levels in the pineal gland. This decline may be one of the manifestations of the pineal gland’s functional involution.

Red blood cell glutathione peroxidase activity in female nulligravid and pregnant rats

BackgroundThe alterations of the glutathione peroxidase enzyme complex system occur in physiological conditions such as aging and oxidative stress consequent to strenuous exercise.MethodsAuthors optimize the spectrophotometric method to measure glutathione peroxidase activity in rat red blood cell membranes.ResultsThe optimization, when applied to age paired rats, both nulligravid and pregnant, shows that pregnancy induces, at seventeen d of pregnancy, an increase of both reactive oxygen substance concentration in red blood cells and membrane glutathione peroxidase activity.ConclusionThe glutathione peroxidase increase in erythrocyte membranes is induced by systemic oxidative stress long lasting rat pregnancy.

Effects of dietary selenium supplementation on serum and liver selenium, serum malondialdehyde and liver glutathione peroxidase activity in rats consuming thermally oxidized sunflower oil

The present study compared the effects of four isocaloric diets containing (1) fresh sunflower oil not supplemented with selenium (Fresh), (2) oxidized sunflower oil not supplemented with selenium (Oxidized), (3) fresh sunflower oil supplemented with 1 ppm selenium as sodium selenite (Fresh + Se), (4) oxidized sunflower oil supplemented with 1 ppm selenium as sodium selenite (Oxidized + Se) on serum MDA concentrations, liver GPx activity and serum and liver selenium contents in growing male Sprague Dawley rats during a period of 43 days. The oxidized oil used was prepared by heating fresh sunflower oil at 180 °C for 48 h. Serum and liver selenium contents and liver GPx activity were significantly higher in the selenium supplemented groups compared to the non-selenium supplemented groups, but these parameters did not differ significantly between the oxidized oil fed groups and the fresh oil fed groups. Serum MDA concentrations increased significantly in the Oxidized group compared to the Fresh group. This suggests that the ingestion of oxidized oil resulted in, in vivo lipid peroxidation. Serum MDA concentrations remained significantly higher even in comparison of the Oxidized + Se group with the Oxidized group. Our results emphasize that the consumption of oxidized oil increases in vivo lipid peroxidation and thus can be deleterious to health. However, we did not observe a significant beneficial effect of selenium supplementation upon the ingestion of thermally oxidized oil on lipid peroxidation.

The influence of calcium channel blockers on the brain free fatty acid level and glutathione peroxidase activity in rats with lithium and pilocarpine‐induced status epilepticus

AbstractThe aim of this study was to investigate possible therapeutic approach to neuronal damage caused by status epilepticus. The effects of the L‐type voltage‐sensitive calcium channel blockers (nimodipine, nicardipine) and NMDA blockers (ifenprodil and MK‐801) on the brain free fatty acid (FFA) level and glutathione peroxidase (GPX) activity in rats with lithium and pilocarpine (LiPi) ‐ induced status epilepticus were examined. Vehicle or various doses of calcium channel and NMDA blockers had been injected i.p. 30 min after the pilocarpine application. Tested doses of nicardipine and MK‐801 did not influence the increase in the brain FFA level. Nimodipine and ifenprodil revealed a tendency to reduce FFA level. The inhibition of L‐type voltage‐sensitive Ca2+ channels or NMDA receptor ‐ associated channels was not sufficient for significant attenuation of an increase in the rat brain FFA content and a decrease GPX activity associated with LiPi ‐ induced status epilepticus. Individual compounds have shown to prevent FFA increase, suggesting some alternative or additional mechanism of action. The prevention of FFA accumulation was not followed by the prevention of GPX decrease indicating the activation of non FFA‐related mechanisms of cell damage.

Effects of dietary zinc and cadmium on tissue selenium concentration and glutathione peroxidase activity in rats fed DL-selenomethionine or sodium selenite.

The effects of dietary zinc (Zn) and cadmium (Cd) on tissue selenium (Se) concentration and glutathione peroxidase (GSH-Px) activity were studied in weanling male Wistar rats. One group of rats was fed a purified diet based on casein and sucrose, and the other rats used in a 2 x 2 x 2 factorial arrangement of treatment were fed this diet supplemented with 0.1 mg Se/kg, either as DL-selenomethionine or sodium selenite and plus 100 mg Zn/kg as zinc sulfate or 5 mg Cd/kg as cadmium chloride or both for 4 weeks. Se concentrations in plasma, erythrocytes, muscle, heart, and liver were significantly elevated by Zn. Cd significantly decreased Se concentration in muscle. Addition of Zn to the diets markedly increased (p less than 0.001) hepatic GSH-Px activity. However, Cd in the diets produced a significant increase (p less than 0.001) in erythrocyte GSH-Px activity. These results indicate that Zn level of marginal deficiency (8.6 mg/kg diet) can decrease Se availability and a small excess of Zn increases Se availability for hepatic GSH-Px activity.

Endrin-induced depletion of glutathione and inhibition of glutathione peroxidase activity in rats

1. Recent studies have shown that endrin induces lipid peroxidation and may produce toxicity through an oxidative stress. We have therefore examined the effect of endrin administration to rats on glutathione content and the activities of glutathione metabolizing enzymes. 2. The oral administration of endrin resulted in dose- and time-dependent decreases in hepatic and renal glutathione content with maximum depletion (90%) occurring in liver at approximately 24 hr post-treatment. 3. Decreases in glutathione content were also observed in lung, brain, spleen and heart. 4. Endrin (4 mg/kg) decreased selenium dependent glutathione peroxidase activity in liver and kidney by 64 and 50%, respectively, while small increases were observed in the activities of glutathione reductase and glutathione S-transferase. 5. The toxicity of endrin may be at least in part related to oxidative tissue damage associated with depletion of glutathione and inhibition of glutathione peroxidase activity.

Effects of Various Dietary Levels of Selenium as Selenite or Selenomethionine on Tissue Selenium Levels and Glutathione Peroxidase Activity in Rats

Weanling rats were fed a basal diet or this diet plus 0.2, 1.0, 2.0 or 4.0 mg/kg selenium (Se) as either selenite or selenomethionine (SeM). Except at the 0.2 mg/kg Se level, Se accumulated in all tissues at higher levels when SeM was fed than when selenite was given, and the magnitude of difference became more pronounced with increasing levels of dietary Se. This was particularly true for muscle and brain. Se levels in whole blood, testes, kidney and lungs were not significantly different between rats fed 0.2 mg/kg Se as selenite or as SeM, but the Se levels in liver, muscle and brain were higher in rats fed SeM. Although the tissue Se concentrations differed markedly, there were no differences in the glutathione peroxidase (GPX) activity in tissues of rats fed SeM rather than selenite. The percentage of Se associated with GPX was lower in all tissues from rats fed SeM than in those from rats fed selenite. These results indicate that the chemical forms of dietary Se can have a marked influence on biological responses, including bioavailability of dietary Se.

Glutathione peroxidase activity in rats poisoned with mercury-vapor and influence of simultaneous administration of selenium

Glutathione peroxidase activity in rats poisoned with mercury-vapor and influence of simultaneous administration of selenium

Dietary selenium, glutathione peroxidase activity, and toxicity of 2,3,7,8-tetrachloro-dibenzo-p-dioxin.

TCDD has been shown to inhibit selenium-dependent glutathione peroxidase activity. The role of selenium in TCDD toxicity is not known. We have therefore examined the effect of TCDD administration on hepatic glutathione peroxidase, aryl hydrocarbon hydroxylase, glutathione reductase, and glutathione S-transferase activities, glutathione content, and lipid peroxidation in rats fed 0, 0.10, and 2.0 ppm dietary selenium. TCDD treatment significantly inhibited selenium-dependent glutathione peroxidase in animals on diets containing 0.10 and 2.0 ppm selenium. The selenium-dependent glutathione peroxidase activities in rats on 0.10 and 2.0 ppm dietary selenium were 8.3-and 4.7-fold greater than in animals fed a diet containing 0 ppm selenium. TCDD administration enhanced hepatic microsomal lipid peroxidation by factors of 4.0, 4.9, and 9.8 in animals fed diets containing 0, 0.10, and 2.0 ppm selenium, respectively. The administration of a lethal dose of TCDD to rats fed diets containing 0, 0.10, and 2.0 ppm selenium resulted in 0, 46, and 7% survival, respectively, after 66 d. Aryl hydrocarbon hydroxylase, glutathione S-transferase, and glutathione reductase activities were induced by TCDD. The results indicate that optimum dietary selenium provides partial protection from the toxic effects of TCDD.

Effects of methylmercury on the erythrocyte glutathione peroxidase activity in rats (author's transl)

Effects of methylmercury on the erythrocyte glutathione peroxidase activity in rats (author's transl)

Effect of Cholesterol Feeding on Tissue Lipid Peroxidation, Glutathione Peroxidase Activity and Liver Microsomal Functions in Rats and Guinea Pigs

The effect of cholesterol feeding on liver and aortic nonenzymatic lipid peroxidation and glutathione peroxidase activities, and on liver microsomal NADPH-dependent lipid peroxidation, codeine hydroxylation and cytochrome P-450 levels was examined in rats and guinea pigs. One percent cholesterol was added to a casein-sucrose-soybean oil basal diet for rats or a stock diet with 2% soybean oil for guinea pigs. The effect of vitamin E and cholestyramine was also examined in some experiments. Cholesterol feeding increased the rate of lipid peroxidation in liver and aortic homogenate both in rats and guinea pigs when fed non-vitamin E supplemented basal diets. Vitamin E supplementation prevented the increase in the aorta, but not as completely in the liver in rats, while the reverse was true in guinea pigs. The effect of cholestyramine was dependent on the level of vitamin E in the diet. Cholesterol feeding decreased glutathione peroxidase activities in rats and guinea pigs. In guinea pigs, cholesterol feeding also markedly decreased liver microsomal NADPH-dependent lipid peroxidation, codein hydroxylation and cytochrome P-450 levels especially when fed non-vitamin E supplemented basal diets. In rats, cholesterol feeding reduced liver microsomal NADPH-dependent lipid peroxidation and in some cases, increased microsomal codeine hydroxylation activities, but had no effect on microsomal cytochrome P-450 levels. Vitamin E supplementation increased liver and serum cholesterol levels in guinea pigs, but had no such effect in rats. Results of this study indicate that cholesterol feeding can result in various metabolic alterations in rats and guinea pigs. The implication of these alterations in atherogenesis requires further investigations.

Glutathione peroxidase activity in rat lens and other tissues in relation to dietary selenium intake

Glutathione peroxidase (E.C. 1.11.1.9: glutathione: H 2O 2 oxidoreductase) activity and selenium concentration were measured in lenses of female rats and their offspring after long-term feeding of either a selenium-supplemented ( 0·1 parts 10 6 ) or selenium-deficient ( < 0·02 parts 10 6 ) diet. Long-term selenium deficiency decreased lens glutathione peroxidase activity in parent rats and their offspring to 15 and 14% respectively of supplemented controls. For comparison to lens, glutathione peroxidase was also measured in liver, heart, lung, erythrocytes, kidney, adrenal, testis, and brain of the offspring. Selenium deficiency caused the enzyme to decrease most dramatically in liver (to 0) and least in brain (to 62% of selenium supplemented controls). Although glutathione peroxidase in lens was lower than that in the other organs assayed, it was among the organs more sensitive to depletion caused by selenium deficiency. A short-term selenium deficiency of 8 weeks in newborn lambs had no effect on lens glutathione peroxidase, but the enzyme in organs such as liver was dramatically decreased. Therefore, an extensive period of selenium deficiency appears necessary to affect lens glutathione peroxidase activity, which probably relates to the relatively slow turnover and slow growth of the lens. The possible role of the seleno-enzyme, glutathione peroxidase, in the prevention of cataracts and the relationship of selenium to vitamin E and sulfur-containing amino acids in this regard are discussed.