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Riboflavin deficiency in man: effects on haemoglobin and reduced glutathione in erythrocytes of different ages.

1. Erythrocytes (RBC) from control and marginally riboflavin-deficient subjects were fractionated into nine fractions using a discrete density gradient. 2. Glutathione reductase (NAD(P)H: glutathione oxidoreductase; EC 1.6.4.2) activity and aspartate aminotransferase (EC 2.6.1.1) activity (with and without the appropriate co-enzymes) reduced glutathione, methaemoglobin, sulphaemoglobin and oxyhaemoglobin and susceptibility to peroxide were measured in RBC in the different fractions. 3. Glutathione reductase and aspartate aminotransferase activities and concentrations of reduced glutathione and oxyhaemoglobin all declined with age, while methaemogloblin, sulphaemoglobin and susceptibility to peroxide increased with age. 4. The only significant differences noted in the RBC from marginally-riboflavin-deficient subjects by comparison with controls, were lower glutathione reductase activities and higher concentrations of methaemoglobin. 5. The role of riboflavin in those systems controlling RBC integrity is discussed.

Aged↗

Purification of NADPH-free glutathione disulfide reductase from human erythrocytes.

Human erythrocyte glutathione disulfide reductase was purified using serially connected 2',5'-ADP-Sepharose 4B affinity and anion-exchange columns. About 11,000-fold purification was achieved with 90% yield. The specific activity of the final preparation was 140 units per milligram of protein. The purified enzyme gave a single band on both native and SDS-PAGE with a subunit mass of 58 kDa. Its pH optimum was 7.20. The Michaelis constants determined at pH 7.4, 37 degrees C, fell within the range of previously reported values [K(m)(NADPH) = 18 microM, at 30-200 microM NADPH; K(m)(GSSG) = 72 microM, at 40-1000 microM glutathione disulfide, both at saturating concentrations of the second substrate]. The affinity eluent NADPH and its oxidized form NADP+ were successfully removed from the enzyme on the ion-exchange column. The purification method developed is very useful when the enzyme source material is scarce (e.g., in preparations from human tissues) and may find further application in the purification of other NAD(P)H-dependent enzymes which might be inactivated by their affinity eluent(s).

Chromatography, Ion Exchange↗

Effects of aldose reductase inhibitors on antioxidant defense in rat and rabbit liver.

Aldose reductase has been implicated in the etiology of diabetic complications, atherosclerosis, and ischemia-reperfusion injury. Aldose reductase inhibitors are known to have species-dependent differences in biotransformation enzyme induction. Whether aldose reductase inhibitors, which have antioxidant potential, alter the oxidative stress pathway is unknown. This study has determined whether four daily ip treatments of either low (10 mg/kg) or high (50 mg/kg) doses of AL-1576 or AL-4114 alter the activities of the antioxidant defense enzymes catalase, glutathione reductase, glutathione peroxidase, superoxide dismutase, and the concentrations of reduced and oxidized glutathione in livers of normal rats and rabbits. There was no change in the concentration of thiobarbituric acid reactive substances in either rat or rabbit livers, indicating that lipid peroxidation was not increased by any treatment. Hepatic catalase, superoxide dismutase, and glutathione peroxidase activities and concentrations of reduced and oxidized glutathione were not significantly altered in rat, though glutathione reductase activity was increased after high doses of both drugs. However, in rabbit liver, glutathione reductase activity decreased in a dose-dependent manner after AL-4114 treatment, while superoxide dismutase and glutathione peroxidase activities decreased only after the low dose of AL-4114. Although AL-4114 and AL-1576 did not directly generate increased lipid peroxidation within normal rat and rabbit livers, some of the enzymes responsible for oxidative defense were altered, particularly in rabbit livers.

Aldehyde Reductase↗

Cyclic nucleotides, thioldisulfide status of proteins, and cellular control processes.

It is shown that cyclic nucleotides can have a variety of effects on cell division, cell shape, cell adhesion, and cell movement, depending on the cells selected and the conditions under which they are used. For example, while CHO cells elongate under the influence of exogenous dibutyryl CAMP, Y-1 adrenal tumor cells round up and polyoma-transformed 3T3 cells show no change in shape. The totality of experience with cyclic nucleotides suggests that where they have been used by cells as control elements involving the four processes listed above, they are superimposed on basic cellular processes that progress in their absence--that is, they must be acting indirectly. In attempting to understand the inhibitory action of methyl xanthines on egg development, we were forced to abandon the idea that they acted through cyclic nucleotides. We found that methyl xanthines inhibited the activation of glutathione reductase and that glutathione oxidizing agents act as mitotic inhibitors. Further, we found that tubulin polymerizability, NAD-kinase activity, and a mitotic apparatus associated Ca+2-ATP-ase were all inhibited by oxidation of some of their sulfhydryls and were activated by reduction of the resulting disulfides. These results are discussed in terms of reported cycles and activations of glutathione reductase (GR) in cells and reports that mixed disulfides of glutathione and proteins can act as substrates for GR. Using the fact that a CAMP-dependent protein kinase has been reported to be activated by glutathione, we have suggested potential sites where sulfhydryl control processes and cyclic nucleotide control processes and cyclic nucleotide control processes may interact in certain restricted cases.

Adenosine Triphosphatases↗

Oxidative stress in chronic renal failure.

This study focuses on the oxidative stress in patients with severe chronic renal failure who are not undergoing dialysis treatment. The erythocyte levels, creatinine clearing and plasma- and cell activities of the following enzymes were determined: glutathione peroxidase (Gpx), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), and glutathione transferase (GT). The concentrations of non-enzyme molecules such as total glutathione in both oxidized and reduced forms, and malonyldialdehyde (MDA) were also measured. The obtained values were compared with those in healthy blood donors of comparable age and social status. The results indicate that chronic renal patients have lower glutathione levels and reduced activities of glutathione peroxidase and of glutathione reductase, while exhibiting elevated levels of malonyldialdehyde and activities of superoxide dismutase, glutathione transferase, and catalase. Finally, creatinine clearing was found to be correlated (p < 0.001) to total (oxidized and reduced) glutathione, Gpx and MDA. These observations may serve to establish a simple protocol for evaluation of renal function.

Biomarkers↗

Silicon-mediated alleviation of Mn toxicity in Cucumis sativus in relation to activities of superoxide dismutase and ascorbate peroxidase.

The effects of exogenous silicon (Si) on plant growth, activities of superoxide dismutase (SOD), guaiacol peroxidase (GPX), ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), glutathione reductase (GR) and catalase, and concentrations of ascorbate and glutathione were investigated in cucumber (Cucumis sativus L.) plants treated with excess manganese (Mn) (600 microM). Compared with the treatment of normal Mn (10 microM), excess Mn significantly increased H2O2 concentration and lipid peroxidation indicated by accumulation of thiobarbituric acid reactive substances. The leaves showed apparent symptoms of Mn toxicity and the plant growth was significantly inhibited by excess Mn. The addition of Si significantly decreased lipid peroxidation caused by excess Mn, inhibited the appearance of Mn toxicity symptoms, and improved plant growth. This alleviation of Mn toxicity by Si was related to a significant increase in the activities of SOD, APX, DHAR and GR and the concentrations of ascorbate and glutathione.

Ascorbate Peroxidases↗

Diquat induces renal proximal tubule injury in glutathione reductase-deficient mice.

Reactive oxygen species (ROS) have been associated with many human diseases, and glutathione (GSH)-dependent processes are pivotal in limiting tissue damage. To test the hypothesis that Gr1(a1Neu) (Neu) mice, which do not express glutathione reductase (GR), would be more susceptible than are wild-type mice to ROS-mediated injury, we studied the effects of diquat, a redox cycling toxicant. Neu mice exhibited modest, dose- and time-dependent elevations in plasma alanine aminotransferase (ALT) activities, 126+/-36 U/l at 2 h after 5 micromol/kg of diquat, but no ALT elevations were observed in diquat-treated C3H/HeN mice for up to 6 h after 50 micromol/kg of diquat. Histology indicated little or no hepatic necrosis in diquat-treated mice of either strain, but substantial renal injury was observed in diquat-treated Neu mice, characterized by brush border sloughing in the proximal tubules by 1 h and tubular necrosis by 2 h after doses of 7.5 micromol/kg. Decreases in renal GSH levels were observed in the Neu mice by 2 h post dose (3.4+/-0.4 vs 0.2+/-0.0 micromol/g tissue at 0 and 50 micromol/kg, respectively), and increases in renal GSSG levels were observed in the Neu mice as early as 0.5 h after 7.5 micromol/kg (105.5+/-44.1 vs 27.9+/-4.8 nmol/g tissue). Blood urea nitrogen levels were elevated by 2 h in Neu mice after doses of 7.5 micromol/kg (Neu vs C3H, 32.8+/-4.1 vs 17.9+/-0.3 mg/dl). Diquat-induced renal injury in the GR-deficient Neu mice offers a useful model for studies of ROS-induced renal necrosis and of the contributions of GR in defense against oxidant-mediated injuries in vivo.

Alanine Transaminase↗

Metallothionein induction related to hepatic structural perturbations and antioxidative defences in roach (Rutilus rutilus) exposed to the fungicide procymidone.

A variety of stresses, hormones, glucocorticoids and cytokines are known to induce metallothioneins (MTs) in animals. The aim of this study was to investigate the effects of chemical stress induced by the dicarboximide fungicide procymidone on hepatic structure, MT content and antioxidative defences (catalase and glutathione reductase activities and glutathione content) in the common fish Rutilus rutilus. Catalase and glutathione reductase activities remained stable throughout the experiment. Four days of exposure to 0.2 or 0.4 mg l(-1) of procymidone induced an obvious increase in liver MT content, perturbation of metal MT contents, and an increase in hepatic glutathione content. After 14 days' exposure, obvious and large structural alterations of the hepatic parenchyma occurred simultaneously with a decrease in MT and glutathione content. These events were interpreted as degeneration of the liver. Fish exposed for 14 days to procymidone and then placed for 14 days in clean water showed nearly complete decontamination of the liver, but MT concentrations remained high. The toxicological significance of these events is discussed.

Animals↗

Glutathione status and sensitivity to GSH-reacting compounds of Escherichia coli strains deficient in glutathione metabolism and/or catalase activity.

The intracellular concentrations of total glutathione, GSSG and protein X S-SG, the total excreted glutathione concentration, and the susceptibility towards GSH-reacting compounds were assayed in strains of Escherichia coli deficient in biosynthesis and/or reduction of glutathione. A deficiency in glutathione reductase displaced the glutathione status towards the oxidized forms. This displacement was more clearly appreciated in strains additionally deficient in glutathione biosynthesis. A deficiency in catalase activity also produced an increase in the oxidation of glutathione. The most severe changes were observed in the concentrations of protein-glutathione mixed disulfides and in the amount of glutathione excreted to the medium. Increased sensitivities towards compounds known to interact with cellular GSH were observed in glutathione reductase deficient strains, although these effects were enhanced in strains additionally deficient in GSH biosynthesis.

Catalase↗

Cystine antagonism of the antibacterial action of lactoperoxidase-thiocyanate-hydrogen peroxide on Streptococcus agalactiae.

Cystine reduction in Streptococcus agalactiae, resulting in sulfhydryl formation, may account for antagonism of the antibacterial effect of lactoperoxidase-thiocyanate-hydrogen peroxide when cystine is present in excess of the amount needed for maximum growth. Accumulation of cystine by S. agalactiae and its reduction to form sulfhydryl compounds were demonstrated. The reduction of cystine appeared to occur by a couple reaction between glutathione reductase and glutathione-disulfide transhydrogenase activity, both of which were found in the supernatant fraction from cell homogenates. NADPH-specific glutathione reductase activity was found in the pellet and supernatant fractions from cell homogenates. Two sulfhydryls were formed for each mole of NADPH used during cystine reduction. The information presented offers a plausible explanation of how cystine, when present in excess of growth needs, may be reduced to generate sulfhydryl compounds which neutralize the antibacterial effect of lactoperoxidase-thiocyanate-hydrogen peroxide on S. agalactiae.

Cystine↗

Glucose-6-phosphate dehydrogenase activity and NADPH/NADP+ ratio in liver and pancreas are dependent on the severity of hyperglycemia in rat.

Hyperglycemia is associated with metabolic disturbances affecting cell redox potential, particularly the NADPH/NADP+ ratio and reduced glutathione levels. Under oxidative stress, the NADPH supply for reduced glutathione regeneration is dependent on glucose-6-phosphate dehydrogenase. We assessed the effect of different hyperglycemic conditions on enzymatic activities involved in glutathione regeneration (glucose-6-phosphate dehydrogenase and glutathione reductase), NADP(H) and reduced glutathione concentrations in order to analyze the relative role of these enzymes in the control of glutathione restoration. Male Sprague-Dawley rats with mild, moderate and severe hyperglycemia were obtained using different regimens of streptozotocin and nicotinamide. Fifteen days after treatment, rats were killed and enzymatic activities, NADP(H) and reduced glutathione were measured in liver and pancreas. Severe hyperglycemia was associated with decreased body weight, plasma insulin, glucose-6-phosphate dehydrogenase activity, NADPH/NADP+ ratio and glutathione levels in the liver and pancreas, and enhanced NADP+ and glutathione reductase activity in the liver. Moderate hyperglycemia caused similar changes, although body weight and liver NADP+ concentration were not affected and pancreatic glutathione reductase activity decreased. Mild hyperglycemia was associated with a reduction in pancreatic glucose-6-phosphate dehydrogenase activity. Glucose-6-phosphate dehydrogenase, NADPH/NADP+ ratio and glutathione level, vary inversely in relation to blood glucose concentrations, whereas liver glutathione reductase was enhanced during severe hyperglycemia. We conclude that glucose-6-phosphate dehydrogenase and NADPH/NADP+ were highly sensitive to low levels of hyperglycemia. NADPH/NADP+ is regulated by glucose-6-phosphate dehydrogenase in the liver and pancreas, whereas levels of reduced glutathione are mainly dependent on the NADPH supply.

Animals↗

Kinetic study of hemoglobin Porto Alegre [beta 9(A6)Ser----Cys] disulfide polymer reduction.

The cleavage of HbPA disulfide polymer by GSH and its indirect cleavage by yeast glutathione reductase, via reduced glutathione is obtained. Decreasing the initial proportion of GSH in the hemolysate increases the formation of HbPA disulfide polymer. In the experimental conditions used, yeast glutathione reductase is unable to perform the direct cleavage of the mixed disulfide of HbPA and GSH, using it as substrate. The reduction of HbPA polymer to tetramers by DTE is analyzed by a pseudo-first-order kinetic and two rate constants are obtained. That of 265 X 10(-3) min-1 should be concerned with one disulfide of the closed ring and one of the open ring structure of dodecamer, while that of 38 X 10(-3) min-1 is related to disulfide reduction of the octamer. The enthalpy of activation values of 8.0 kcal.mol-1 an 17.4 kcal.mol-1 obtained, from the Arrhenius plot, for the "fast" and "slow" rate disulfide reduction, respectively, are indicative that a strong conformational strain of S--S bonds in the closed ring structure is maintained. The entropy of activation values of 24 e.u. and 52 e.u. are found for the activation of disulfides from dodecamers and octamers, respectively.

Brazil↗

Metabolic effects of antisickling amounts of nitrogen and nor-nitrogen mustard on rabbit and human erythrocytes.

Nitrogen mustard (NH2) and Nor-nitrogen mustard (Nor-HN2) both inhibit the polymerization of deoxyhemoglobin S in solution and in intact erythrocytes. Metabolic studies were undertaken to determine the feasability of an extracorporeal treatment with these or related agents. Glucose utilization, hexose monophosphate shunt activity, methemoglobin reduction, and incubation with acetylphenylhydrazine for Heinz body formation were performed, as well as specific assays for hexokinase, pyruvate kinase, glucose-6-phosphate dehydrogenase, glutathione reductase, ATP, reduced glutathione (GSH), and survival of autologous mustard-treated cells in rabbits. HN2 was found to enter red cells rapidly and bind to intracellular contents. Metabolic studies revealed no significant inhibition or alteration of function by Nor-HN2 at 10 mg/ml of whole blood. Rabbit red cell survival was also normal. HN2, however, inhibited glutathione reductase and blocked the free sulfhydryl group of GSH by forming serveral addition products of alkylated GSH. Heinz body test with acetylphenylhydrazine became positive in HN2-treated cells, and rabbit red cell survival was shortened considerably in the concentration range used to inhibit sickling. Ascorbic acid stimulation of the hexose shunt pathway was inhibited by HN2, but methylene blue stimulation remained unaffected. 14-C-HN2 remains bound to red cells in vivo, and the disappearance of radioactivity is similar to that found with 14-C-DFP (disopropylfluorophosphate). Oxygen affinity of both HN2 and Nor-HN2 treated human red cells remains virtually the same as that found in control samples. It is concluded that Nor-HN2 may be a suitable agent for an extracorporeal therapy, and that each mustard needs to be evaluated individually for its antisickling effects and its suitability for extracorporeal use.

Animals↗

Anti-oxidant enzymes in Cryptosporidium parvum oocysts.

Oocysts of Cryptosporidium parvum showed relatively low levels of SOD activity. The SOD which had a pI of 4.8 and an approximate molecular weight of 35 kDa appeared to be iron dependent. Catalase, glutathione transferase, glutathione reductase and glutathione peroxidase activity could not be detected, nor could trypanothione reductase. No NADH or NADPH oxidase activity could be detected, nor could peroxidase activity be demonstrated using o-dianisidine, guaiacol, NADPH or NADH as co-substrates. However, an NADPH-dependent H2O2 scavenging system was detected in the insoluble fraction.

Animals↗

In vitro haematotoxic effects of three methylated hydroxylamines.

Hydroxylamine (HYAM, HONH2) and some of its derivatives are known to cause erythrotoxic effects both in vitro and in vivo. Previous studies have shown that the primary in vitro effect of HYAM and O-ethyl hydroxylamine (OEH) is methaemoglobin formation, leading to liberation of free radicals which cause lipid peroxidation, enzyme inhibitions and glutathione depletion. By contrast, N-substituted N,O-dimethyl hydroxylamine (NODMH), primarily induces impairment of glucose 6-phosphate dehydrogenase (G6PDH) and glutathione reductase (GR). The oxidative potency of HYAM and the O-derivative was larger than the potency of the N,O-derivative. This seemed to indicate that attachment of an alkyl group to the nitrogen atom of hydroxylamine leads to decreased reactivity. To achieve a better understanding of the structure activity relationship for hydroxylamines three methylated derivatives were tested: N-methyl hydroxylamine (NMH). N-dimethyl hydroxylamine (NDMH) and O-methyl hydroxylamine (OMH). We were also interested in the erythrotoxic potency of OMH which recently entered industrial production. Methaemoglobin formation, high release of lipid peroxidation products, inhibition of NADPH methaemoglobin reductase and glutathione S-transferase (GST) and depletion of total glutathione (GT) were seen for OMH. The reducing enzymes G6PDH and GR were not impaired by OMH. These findings for OMH are consistent with the proposed mechanism for O-derivatives. Since both the effects caused by OMH and its potency are comparable to those of HYAM and OEH this indicates that possible occupational exposure to this compound may be approached similarly to HYAM and OEH. NMH only inhibited G6PDH and GR activity, which is fully in accord with the proposed mechanism for N-substituted derivatives of HYAM. However, NDMH a double N-substituted compound, caused a strikingly different scheme of reactivity inhibition of G6PDH but not of GR, severe methaemoglobin formation, only little lipid peroxidation and some impairment of NADPH methaemoglobin reductase. This study confirms that O-derivatives of HYAM are potent haemoglobin oxidators, leading to other oxidative effects. The main effect was confirmed for single N-derivatives as inhibition of the two protective enzymes G6PDH and GR. However, the results for NDMH indicate that this simple classification of O-derivatives and N-derivatives has to be extended for double N-substituted compounds which give a mixture of effects.

Cytochrome-B(5) Reductase↗

Activities of antioxidant and redox enzymes in human normal hepatic and hepatoma cell lines.

The cellular defense system (including glutathione, glutathione-related enzymes, antioxidant and redox enzymes) plays a crucial role in cell survival and growth in aerobic organisms. To understand its physiological role in tumor cells, the glutathione content and related enzyme activities in the human normal hepatic cell line, Chang and human hepatoma cell line, HepG2, were systematically measured and compared. Superoxide dismutase, catalase, and glutathione peroxidase activities are 2.8-, 4.3-, and 2.9-fold higher in HepG2 cells than in Chang cells. Total glutathione content is also about 1.4-fold higher in HepG2, which is supported by significant increases in gamma-glutamylcysteine synthetase and glutathione synthetase activities. Two other glutathione-related enzymes, glutathione reductase and gamma-glutamyltranspeptidase, are upregulated in HepG2 cells. However, thioredoxin reductase and glutathione S-transferase activities are significantly lower in HepG2 cells. These results propose that defense-related enzymes are largely modulated in tumor cells, which might be linked to their growth and maintenance.

Antioxidants↗

Differential response of cellular antioxidant mechanism of liver and kidney to arsenic exposure and its relation to dietary protein deficiency.

The effect on antioxidant defense system of liver and kidney of sub-acute i.p. exposure to sodium arsenite (3.33 mg/kg b.w. per day) for 14 days was studied in male Wistar rats fed on an adequate (18%) or a low (6%) protein diet. Following arsenic treatment, liver showed significantly enhanced concentration of glutathione and increased activities of glutathione reductase and glutathione-S-transferase on either of the dietary protein levels. Liver glutathione peroxidase and glucose-6-phosphate dehydrogenase activities increased significantly on an adequate protein diet while glutathione peroxidase activity decreased significantly on a low-protein diet. Lipid peroxidation and superoxide dismutase activity of liver remained unaltered on either of the dietary protein levels. On the other hand, kidney of arsenic-treated rats receiving either of the dietary protein levels showed significantly increased lipid peroxidation and decreased superoxide dismutase and catalase activities. Kidney glutathione content and glutathione reductase activity remained unaltered while glutathione peroxidase activity increased and glutathione-S-transferase activity decreased significantly on a low-protein diet following exposure to arsenic. On an adequate protein diet glucose-6-phosphate dehydrogenase activity in kidney, however, became significantly elevated following arsenic treatment. In Wistar rats, after 14 days of treatment with 3.33 mg As/kg b.w. i.p. the kidney seemed to be more sensitive to arsenic, and liver appears to be protected more by some of the antioxidant components, such as, glutathione, glutathione-S-transferase and glucose-6-phosphate dehydrogenase. It appears that low-protein diet influences the response of some of the cellular protective components against arsenic insult but does not lead to unique findings.

Journal Article↗

The role of free radicals in leaf senescence.

Decreased catalase activity is a consistent feature of leaf senescence. Although not as well documented, superoxide dismutase appears generally to decrease during leaf senescence. These changes suggest that free radical levels are likely to be higher in senescing tissues. The hydrogen peroxide-scavenging ability of chloroplasts due to the activity of the enzymes ascorbate peroxidase, dehydroascorbate reductase and glutathione reductase appears to be established although there is no information on changes in levels of these enzymes in response to leaf senescence. In plants, unlike mammals, the direct reaction of glutathione with H2O2, catalysed by glutathione peroxidase, appears to be only a minor means of scavenging hydrogen peroxide. Senescence appears to be correlated with increases in lipid peroxidation and membrane permeability. The findings reviewed in this paper lend general support to the view that free radicals play a significant role in the multifactorial syndrome which constitutes leaf senescence.

Aging↗