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PubMed2005

Protective activities of stilbene glycosides from Acer mono leaves against H2O2-induced oxidative damage in primary cultured rat hepatocytes.

In our previous study, we isolated two new hepatoprotective stilbene glycosides, 5-O-methyl-(E)-resveratrol 3-O-beta-D-glucopyranoside (MRA) and 5-O-methyl-(E)-resveratrol 3-O-beta-D-apiofuranosyl-(1-->6)-beta-D-glucopyranoside (MRAG), from the methanolic extract of Acer mono leaves. Thereby, we have attempted to elucidate the hepatoprotective mechanism of these compounds, focusing on antioxidative effects, using hydrogen peroxide (H2O2)-injured primary cultures of rat hepatocytes. Both MRA and MRAG showed potent hepatoprotective activities in pretreatment but showed little effects in posttreatment. In addition, they increased the glutathione (GSH) level in the normal control cultures and significantly prevented the depletion of GSH in H2O2-injured primary cultured rat hepatocytes. Moreover, these compounds significantly restored the level of GSH depleted by buthionine sulfoximine or diethylmaleate in the presence or absence of H2O2. Furthermore, these compounds preserved the activities of antioxidant enzymes such as superoxide dismutase, glutathione reductase, and glutathione peroxidase reduced by H2O2 insults. Meanwhile, MRA and MRAG showed moderate scavenging effects with IC50 values of 103.6 and 80.5 microM, respectively, as determined by 1,1-diphenyl-2-picryl-hydrazyl free radical scavenging activity. Taken together, these results suggest that MRG and MRAG exert significant hepatoprotective activities against H2O2-induced hepatotoxicity by maintaining the antioxidative defense system rather than scavenging free radicals.

Acer↗

PubMed2000

Chronic diarrhea impairs intestinal antioxidant defense system in rats at weaning.

The aim of the present study was to evaluate the influence of severe protein-energy malnutrition on the antioxidant defense system in the small and large intestine in rats at weaning. Chronic diarrhea and the subsequent malnutrition were induced by oral intake of a lactose-enriched diet. Twenty rats were weaned at 21 days of age, and the control group was fed a semipurified synthetic diet for two weeks. The malnourished group was fed the same diet but carbohydrates were replaced by lactose, and they developed diarrhea one day after. Rats were killed, and macroscopic and histological features were analyzed, DNA content was measured, and alkaline phosphatase, myeloperoxidase, and gamma-glutamyltranspeptidase activities were determined to assess the degree of intestinal injury. Glutathione levels as well as the activities of intestinal glutathione transferase, glutathione reductase, total glutathione peroxidase, selenium-dependent glutathione peroxidase, superoxide dismutase, and catalase were measured to study the antioxidant defense system. Malnourished rats showed loss of body weight and an increase in length and weight in jejunum and ileum, while no significant changes were observed in colon. Epithelial cells showed fewer and shorter microvilli, larger mitochondria with low inner density and loss of cristae, dilated endoplasmic reticulum, and Golgi apparatus. The protein-to-DNA ratio was higher in the jejunum, ileum, and colon of malnourished rats. Glutathione levels decreased 40% in jejunum and 50% in colon of malnourished rats. A 40-50% decrease in the activity of all the enzymes of the antioxidant defense system was observed in the jejunum and ileum of malnourished rats, while only catalase and glutathione transferase activities decreased 50% in colon. These results suggest that early chronic diarrhea and severe protein-energy malnutrition impair the antioxidant defense system in both the small and large intestine, which may have a role in the pathogenesis and maintenance of the vicious circle of malabsorption-diarrhea-malnutrition in infancy.

Animals↗

PubMed2002

Antioxidant/restorative effects of calcined gold preparations used in Indian systems of medicine against global and focal models of ischaemia.

Stroke, or ischaemic brain damage, is of great geriatric importance being the third most common cause of death after cancer and heart diseases in developed countries. Despite such high frequency, its management has received inadequate attention. Many studies have shown the role of free radicals in the pathogenesis of ischaemic brain damage. Search for safe and effective antioxidant and free radial scavenger agents, therefore, appear to be a promising approach for stroke therapy. Gold, widely used in modern medicine for the treatment of rheumatoid arthritis, is highly valued for various medicinal uses in Indian systems of medicine. Traditional gold preparations are attributed with tonic/rejuvenating and antioxidant properties. Our earlier studies revealed interesting analgesic, immunostimulant, adaptogenic and glycogen sparing properties in these preparations, but their effects in cerebral ischaemia have not been investigated. This prompted us to initiate the present study using global and focal models of ischaemia in albino rats. Enzymatic parameters (lipid peroxidase, reduced glutathione, catalase, glutathione reductase, glutathione-S-transferase, glutatione peroxidase, superoxide dismutase, and glucose-6-phosphate dehydrogenase) were employed to assess ischaemic brain damage and its modulation. Significant restoration of altered values to near normal levels by Ayurvedic Swarna Bhasma and Unani Kushta Tila Kalan (25 mg/kg, orally for 10 days), suggest potentials for gold preparations in cerebrovascular diseases. The preparations deserve more scientific attention for possible therapeutic exploitation.

Animals↗

PubMed2003

Aluminum-induced pro-oxidant effects in rats: protective role of exogenous melatonin.

In recent years, it has been suggested that oxidative stress is a feature of Alzheimer's disease in which aluminum (Al) could exacerbate oxidative events. The goal of the present study was to assess in rats the pro-oxidant effects induced by Al exposure, as well as the protective role of exogenous melatonin. Two groups of male rats were intraperitoneally injected with Al only or melatonin only, at doses of 5 and 10 mg/kg/day, respectively for 8 wk. During this period, a third group of animals received Al (5 mg/kg/day) and melatonin (10 mg/kg/day). At the end of the treatment period, rats were anesthesized and arterial blood was obtained. Thereafter, animals were killed and liver and brain (cortex, hippocampus and cerebellum) were removed. These tissues were processed to examine oxidative stress markers: glutathione transferase (GST), reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), thiobarbituric acid reactive substances (TBARS), as well as protein content. Samples of these tissues were also used to determine Al, Fe, Mn, Cu and Zn concentrations. The results show that Al exposure promotes oxidative stress in different neural areas, including those in which Al concentrations were not significantly increased. The biochemical changes observed in neural tissues show that Al acts as pro-oxidant, while melatonin exerts an antioxidant action in Al-treated animals. The protective effects of melatonin against cellular damage caused by Al-induced oxidative stress, together with its low toxicity, make melatonin worthy of investigation as a potential supplement to be included in the treatment of neurological disorders in which the oxidative effects must be minimized.

Aluminum↗

PubMed1998

Influence of aminoguanidine on parameters of liver injury and regeneration induced in rats by a necrogenic dose of thioacetamide.

1. When aminoguanidine, a nucleophilic hydrazine compound, was administered to rats (50 mg kg(-1) body wt) 30 min before a necrogenic dose of thioacetamide (500 mg kg(-1) body wt), significant changes related to liver injury and hepatocellular regeneration were observed. 2. The extent of necrosis was noticeably less pronounced, as detected by the peak of serum aspartate aminotransferase activity. Depletion of hepatic glutathione (GSH) and the increase in malondialdehyde concentration as markers of oxidative stress, produced by thioacetamide metabolism, were significantly diminished. However, the activity of microsomal FAD monooxygenase, the system responsible for thioacetamide oxidation, did not show significant alterations. Antioxidant enzyme systems involved in the glutathione redox cycle, such as glutathione reductase and glutathione peroxidase activities, slightly decreased following aminoguanidine pretreatment. 3. Primary cultures of peritoneal macrophages from control rats, when incubated in the presence of serum collected following thioacetamide intoxication, showed a significant decrease in nitric oxide (NO) release at 24 h, that was more pronounced in the group pretreated with aminoguanidine. However, the sharp and progressive increase in macrophage NO release, when incubated in the presence of serum obtained at 48, 72 and 96 h, were increased by aminoguanidine-pretreatment. 4. The cell population involved in DNA synthesis sharply increased in both groups at 48 h of intoxication, although the values at 0, 24, 72 and 96 h were markedly higher in the group pre-treated with aminoguanidine. Polyploidy at 72 and 96 h of intoxication was delayed by the effect of aminoguanidine and a progressive increase in the hypodiploid hepatocyte population, which reached 16% of the total at 96 h, was observed. 5. These results indicate that a single dose of aminoguanidine before thioacetamide administration, markedly diminished the severity of the liver injury by decreasing oxidative stress and lipoperoxidation, but hepatocellular regeneration was apparently unaffected probably due to an enhanced mitogenic activity.

Animals↗

PubMed1983

Relative contributions of thioltransferase-and thioredoxin-dependent systems in reduction of low-molecular-mass and protein disulphides.

Two enzyme systems capable of reducing disulphide bonds both in low-Mr compounds and in polypeptides and proteins exist. One consists of thioltransferase in combination with reduced glutathione and glutathione reductase, and the second consists of thioredoxin in combination with thioredoxin reductase. Their relative effectiveness in catalysing disulphide reduction of various substrates in rat liver cytosol was evaluated in the present study. The thioltransferase-dependent system was found to be more efficient in reducing small molecules. Insulin was most effectively reduced by the thioredoxin system. Bovine trypsin was a better substrate for thioltransferase, and partially proteolysed bovine serum albumin was equally good for the two systems. Thus, in the case of protein disulphide bonds, the nature of the particular substrate used determines which of the two reducing systems is the more important.

Animals↗

PubMed2001

Progressive apoptosis in chorion laeve trophoblast cells of human fetal membrane tissues during in vitro incubation is suppressed by antioxidative reagents.

Previously, we demonstrated apoptotic cell death in the chorion laeve trophoblast layer of human fetal membrane tissues during the late stages of pregnancy, the progression of apoptosis during incubation in vitro, and its suppression by a low concentration of glucocorticoid hormones. We now report examination of mRNA expression of inflammatory cytokines [interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha] and antioxidative enzyme genes [heme oxygenase 1, catalase, Mn-superoxide dismutase (SOD), Cu/Zn-SOD, glutathione S-transferase, glutathione reductase and glutathione peroxidase] and apoptosis-related genes during in vitro progression of apoptosis with or without glucocorticoid by a reverse transcription/PCR method. It was shown that the mRNA levels increased in chorion laeve tissue for each cytokine examined and for catalase, heme oxygenase 1 and Mn-SOD in direct correlation with the in vitro incubation period. By Western blotting the existence of Mn-SOD protein, and its slight increase with incubation time, was also shown. The investigation of the influence of antioxidative reagents [pyrrolidine dithiocarbamate (PDTC), N-acetyl-l-cysteine (NAC) and nordihydroguaiaretic acid (NDGA)] on DNA fragmentation showed that DNA fragmentation in chorion laeve tissues was inhibited by approximately 50% in the presence of 1 mm PDTC, 30 mm NAC and 1 mm NDGA. These results suggest that apoptotic cell death of the trophoblast layer of chorion tissues may be induced through intracellular oxidative stress at the stage of parturition.

Acetylcysteine↗

PubMed1998

Pterins in human hair follicle cells and in the synchronized murine hair cycle.

Human dermal papilla cells (HDPC) express mRNA for the key enzymes for de novo synthesis/recycling and regulation of the pterin (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin (6BH4). HDPC had significantly higher enzyme activities and 6BH4 levels in a comparative study with dermal fibroblasts, epidermal melanocytes, and keratinocytes under in vitro conditions. In addition, a significantly more rapid uptake of 14C-L-phenylalanine was demonstrated in HDPC compared with fibroblasts, whereas the differences in turnover to L-tyrosine were insignificant, suggesting a pooling of L-phenylalanine in HDPC. These results suggested that HDPC driven 6BH4 synthesis could be of major functional importance in the hair cycle. In order to follow this hypothesis in vivo, expression of enzyme activities and levels of the produced cofactor during the synchronized hair cycle were determined employing the murine model C57BL/6. These data revealed a significantly increased de novo synthesis for 6BH4 via GTP-cyclohydrolase I concomitant with high levels of 6BH4, and the induction of phenylalanine hydroxylase activities during the telogen/early anagen stage (days 0-1). Pterin levels and enzyme activities fall on day 3 and plateau during the rest of the entire cycle. In addition, thioredoxin reductase and glutathione reductase activities were measured, where the latter enzyme remained constant but thioredoxin reductase activities showed a biphasic behavior. The first peak coincided with the induction of 6BH4 de novo synthesis at the beginning of the hair cycle. The second peak was observed at mid-anagen, when melanogenesis takes place. Taken together, our results show the presence of autocrine pterin synthesis/recycling in human hair follicle cells under in vitro conditions, and a possible role for 6BH4 in the synchronized murine hair cycle.

Animals↗

PubMedDate not supplied

Glycolytic enzymes of stored granulocytes.

A marked reduction of granulocyte chemotactic function accompanies the storage of granulocyte concentrates. Since chemotaxis is energy dependent, we studied energy metabolism in stored neutrophils. We and others have reported that stored neutrophils have a defect in their energy metabolism. We found that defective adenosine triphosphate maintenance in stored neutrophils was occult in resting cells, but was unmasked by an energy-intensive stimulus, phagocytosis. In studies reported here, we sought to determine if defective adenosine triphosphate maintenance during granulocyte storage was related to altered glycolytic enzyme activity. We studied the activity of glycolytic enzymes in fresh and stored, resting and stimulated (opsonized zymosan) neutrophils. The following enzyme activities showed no major changes during storage, in resting or stimulated neutrophils: hexokinase, phosphofructokinase, aldolase, glucose phosphate isomerase, triose phosphate isomerase, glyceraldehyde phosphate dehydrogenase, phosphoglycerate kinase, phosphoglyceromutase, enolase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, glutathione reductase, and glutathione peroxidase. In contrast, pyruvate kinase activity consistently increased during storage. In 6 units, pyruvate kinase activity increased by 75 percent after 24 hours of storage at room temperature and by 198 percent after 48 hours. The storage-associated increase in pyruvate kinase activity was not inhibited by cycloheximide. Stimulation of neutrophils by phagocytosis of opsonized zymosan also produced striking increases in the pyruvate kinase activity of both fresh and stored cells. Additional studies indicated that the increases in pyruvate kinase activity observed during storage and after phagocytosis were associated with an increase in the availability of pyruvate kinase activity in the supernatant fraction of neutrophil sonicates. Total pyruvate kinase activity in sonicates of neutrophils was unchanged by storage or particle ingestion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗

PubMed2005

Ventricular arrhythmias following exposure of failing hearts to oxidative stress in vitro.

INTRODUCTION: There is experimental evidence that heart failure (HF) is an oxidative stress and that HF myocytes may be damaged by oxygen-derived free radicals. However, the arrhythmogenicity of these radicals has not been studied in HF. METHODS AND RESULTS: Isolated perfused hearts were obtained from sham-operated (SHAM, n = 6), and fast pacing (250 ms, 2 weeks)-induced heart failure porcines (HF, n = 8). Epicardial conduction was mapped in the longitudinal and transverse directions and ventricular arrhythmias were closely monitored after perfusion of 100, 300, and 1000 micromol/L H(2)O(2). Left ventricular epicardium was sampled for action potentials recordings in the same conditions. Myocardial levels of thiobarbituric acid reactive substances and antioxidant enzymatic capacity were also assessed. Epicardial conduction velocities were unaffected by H(2)O(2) in both groups. Isolated ventricular premature beats and runs of slow ventricular rhythm with H(2)O(2) more frequently occurred in HF compared to SHAM despite an increased antioxidant capacity including Cu/Zn and Mn superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase. Sustained arrhythmias were not observed. Higher thiobarbituric acid reactive substances levels were found in HF confirming endogenous oxidative stress. Action potential duration at plateau level was increased following H(2)O(2) in SHAM but not in HF epicardial fibers where a toxic effect developed at 1000 micromol/L. CONCLUSION: Oxidative stress with concomitant increase in antioxidant capacity develops in this HF model. There is a greater proclivity to oxidative stress-mediated arrhythmias in HF. These arrhythmias are mainly extrasystoles or slow ventricular rhythms and not dependent on abnormal myocardial conduction.

Action Potentials↗

PubMed1975

Chicken neutrophils: oxidative metabolism in phagocytic cells devoid of myeloperoxidase.

Polymorphonuclear leukocytes isolated from chicken peritoneal exudates have been found to catalyze cyanide-insensitive stimulation of respiration and the hexose monophosphate shunt upon exposure to heat-inactivated Staphylococcus aureus. However, there was no demonstrable formate oxidation concomitant with phagocytosis in either the presence or absence of exogenous catalase. Moreover, chicken polymorphonuclear leukocytes failed to oxidize scopoletin concomitant with phagocytosis in the presence of horseradish peroxidase. While oxygen uptake was increased 2- to 3-fold by the stimulus of phagocytosis, the oxidation of [1-(14)C]glucose was increased approximately 20-fold. The cells contain two mechanisms, a glutathione reductase-glutathione peroxidase system and an NADPH-NAD+ transhydrogenase, each of which is present in sufficient capacity to accommodate the enhanced shunt activity. Although chicken polymorphonuclear leukocytes were found to possess a substantial capacity to catalyze the cyanide-insensitive oxidation of either NADH or NADPH, the total or specific activities of such processes were not demonstrably affected by phagocytosis.

Animals↗

PubMed1999

Genetic analysis of glutathione peroxidase in oxidative stress response of Saccharomyces cerevisiae.

Three glutathione peroxidase homologs (YKL026C, YBR244W, and YIR037W/HYR1) were found in the Saccharomyces Genome Database. We named them GPX1, GPX2, and GPX3, respectively, and we investigated the function of each gene product. The gpx3Delta mutant was hypersensitive to peroxides, whereas null mutants of the GPX1 and GPX2 did not show any obvious phenotypes. Glutathione peroxidase activity decreased approximately 57 and 93% in the gpx3Delta and gpx1Delta/gpx2Delta/gpx3Delta mutants, respectively, compared with that of wild type. Expression of the GPX3 gene was not induced by any stresses tested, whereas that of the GPX1 gene was induced by glucose starvation. The GPX2 gene expression was induced by oxidative stress, which was dependent upon the Yap1p. The TSA1 (thiol-specific antioxidant) gene encodes thioredoxin peroxidase that can reduce peroxides by using thioredoxin as a reducing power. Disruption of the TSA1 gene enhanced the basal expression level of the Yap1p target genes such as GSH1, GLR1, and GPX2 and that resulted in increases of total glutathione level and activities of glutathione reductase and glutathione peroxidase. However, expression of the TSA1 gene did not increase in the gpx1Delta/gpx2Delta/gpx3Delta mutant. Therefore, de novo synthesis and recycling of glutathione were increased in the tsa1Delta mutant to maintain the catalytic cycle of glutathione peroxidase reaction efficiently as a backup system for thioredoxin peroxidase.

Amino Acid Sequence↗

PubMed2004

Thiol metabolism in preterm infants during the first week of life.

BACKGROUND: Oxidative stress is implicated in the pathogenesis of several complications of prematurity. The glutathione cycle is one of the most important intracellular antioxidant systems. The synthesis of glutathione may not be adequate in preterm neonates because of the low levels of cysteine available. The aim of this study was to evaluate cysteine and glutathione metabolism during the first week of life in preterm infants. METHODS: Plasma and erythrocyte thiol concentrations were measured in 78 preterm infants with a birthweight of 500-1500 g, and erythrocyte glutamate-cysteine ligase (GCL), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferases (GST) and glucose 6-phosphatedehydrogenase (G6PDH) in 26 infants with a birthweight of 1000-1500 g. RESULTS: The mean (SD) plasma glutathione concentration increased from day 0 to day 1 (14.9 (7.1) vs. 27.7 (11.9) micromol/L, p < 0.001), and then decreased. The plasma cysteine concentration changed in the opposite direction (172 (59) vs. 129 (42) micromol/L, p < 0.01). In infants with respiratory distress syndrome (RDS) the mean plasma glutathione concentration, but not cysteine, was lower on day 0 compared with infants without RDS (11.7 (5.2) vs. 21.4 (5.6) micromol/L, p < 0.01). Erythrocyte glutathione concentration decreased during the first week of life, whereas erythrocyte cysteine concentration increased significantly from day 3 to day 7 (p < 0.01). Erythrocyte cysteine and glutathione concentrations had a positive correlation. The GCL and GR activities did not change, but GST and G6PDH activities decreased during the first week (p < 0.01). GPx activity decreased until day 3 (p < 0.01) and was higher on day 0 and day 1 in infants with RDS. CONCLUSIONS: Very low birthweight infants have an initial increase in plasma glutathione and initial decrease in plasma cysteine level during the first week of life, and also a positive correlation between erythrocyte cysteine and glutathione levels.

Cysteine↗

PubMed1998

Hydrogen peroxide formation in platelets of patients with non-insulin-dependent diabetes mellitus.

A group of 29 patients with non-insulin-dependent diabetes mellitus (NIDDM) was compared with a group of 19 patients who had good glycemic control for platelet activity and hydrogen peroxide formation. NIDDM patients showed platelet hyperactivity in response to low ADP concentrations. In addition, stimulated platelets from untreated NIDDM patients produced more hydrogen peroxide than platelets of treated and normal subjects. Hydrogen peroxide accumulation was not related to modification of the enzymatic systems involved in its synthesis and break-down. The specific activities of NAD(P)H cytochrome C reductase, catalase, glutathione peroxidase and glutathione reductase were not different between patients and healthy subjects. It is likely that the platelet intracellular elevation of reactive oxygen free-radicals could play an important role in the vascular complications and thrombotic risk that is often present in NIDDM patients.

Journal Article↗

PubMed1987

Some aspects of glutathione metabolism in ataxia-telangiectasia fibroblasts.

Levels of glutathione (GSH) and two enzymes involved in GSH metabolism, glutathione reductase (GR) and glutathione-S-transferase(s) (GST), were measured in four SV40-transformed human fibroblast cell lines. MRC5-V1 and GM0637, derived from normal individuals, had mean GSH levels of 4.2 and 6.5 nmoles/10(6) cells, respectively. TAT2SF and AT5BIVA, both from ataxia-telangiectasia (A-T) patients, respectively had 6.5 and 4.2 nmol/10(6) cells, indicating that basal GSH levels were similar in A-T and normal cells. There was some variation in GST activity among the four cell lines but deficiency in this enzyme cannot be associated with radiosensitivity in A-T. When GR activity was measured, A-T cells had approximately 82 per cent of the mean normal activity. Though statistically significant, (P = 0.05), this small deficiency could be due to chance and is unlikely to be responsible for the radiosensitive phenotype of A-T.

Ataxia Telangiectasia↗

PubMed2000

Evaluation of oxidative stress in some cases of argimone oil poisoning during a recent outbreak of epidemic dropsy in India.

The study was designed to evaluate the oxidative stress and modulation of anti-oxidant enzymes in 10 accidental argimone oil poisoning cases admitted in a hospital in Delhi, India during a recent outbreak of epidemic dropsy in 1998. Serum malondialdehyde (MDA) level, oxygen free-radical scavenging enzymes such as superoxide dismutase (SOD) and catalase (CAT), and glutathione (GSH) and related enzymes, e.g. glutathione reductase (GR), glutathione peroxidase (GPx), gamma glutamyl transpeptidase (GGT) and glutathione-S-transferase (GST) in erythrocytes were assayed. The sanguinarine level in serum was measured by high-performance liquid chromatography. The serum MDA level was higher and the GSH level in erythrocytes was lower in argimone oil poisoning cases than those in controls. There was a significant decrease in SOD and GPx activities in erythrocytes of epidemic dropsy cases but no changes were observed in CAT, GR and GST assay. The depletion of GSH in erythrocytes, serum MDA level and clinical severity were dependent on serum sanguinarine level. The results indicate that sanguinarine (argimone oil) poisoning creates an oxidative stress in humans. The oxidative stress and differential modulation of anti-oxidant enzymes by sanguinarine might play a pathogenic role in epidemic dropsy, which suggests the incorporation of anti-oxidant drugs in the treatment protocol of the disease.

Chromatography, High Pressure Liquid↗

PubMed1997

The effect of selenium on antioxidant system in erythrocytes and liver of the carp (Cyprinus carpio L.)

The effect of selenium-supplemented diet (sodium selenate and selenium yeast) on antioxidant in erythrocytes and liver of the carp (Cyprinus carpio L.) fingerlings was studied. With this goal, the activities of glutathione peroxidase (GSH-Px), catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR) and glutathione-S-transferase (GST), as well as glutathione (GSH + GSSG) level, were determined. In the group supplemented with sodium selenate, no significant changes in the activity of the above enzymes were recorded in both the erythrocytes and in the liver, with the exception of GST activity that was significantly reduced in the plasma compared with the controls. Glutathione content was at the control level. In the group supplemented with selenium-yeast, the activities of GSH-Px, CAT, and SOD were significantly increased in erythrocytes, whereas GST activity and plasma content of GSH + GSSG were reduced compared with the controls. At the same time, the activities of hepatic SOD and GST were increased compared with the controls. These results demonstrate that organically bound selenium (selenium-yeast) acts more efficiently on antioxidant system of the carp fingerlings than inorganic selenium salts.

Animals↗

PubMed1998

Hexokinase, glucose-6-phosphate dehydrogenase and antioxidant enzymes in diabetic reticulocytes: effects of insulin and vanadate.

Experimentally induced diabetic rats were treated separately with insulin and vanadate. The activities of hexokinase (HK) and glucose-6-phosphate dehydrogenase (G-6PDH) were increased in reticulocyte hemolysate isolated from the diabetic rats and were restored to normal levels by insulin. The restoration was not detected in vanadate treated diabetic animals. The enzymes of glutathione metabolism namely glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-s-transferase (GST) exhibited increases in their activities with diabetes and were restored to almost control values by insulin treatment. Vanadate given to diabetic animals further increased GPx, and GST. The level of superoxide dismutase(SOD) decreased in the reticulocytes of diabetic rats and catalase (CAT) was unchanged. Both CAT and SOD had normal values when the diabetic rats were treated with insulin and vanadate. It is proposed that vanadate may cause an increase in the activity of GR which may stimulate glucose transporters and glucose metabolism.

Animals↗