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• W2001993344 abstract "Chronic hemodialysis (HD) patients increase erythrocyte susceptibility to hemolysis and impair cell survival. We explored whether electrolyte-reduced water (ERW) could palliate HD-evoked erythrocyte impairment and anemia. Forty-three patients undergoing chronic HD were enrolled and received ERW administration for 6 month. We evaluated oxidative stress in blood and plasma, erythrocyte methemoglobin (metHb)/ferricyanide reductase activity, plasma metHb, and proinflammatory cytokines in the chronic HD patients without treatment (n=15) or with vitamin C (VC)- (n=15), vitamin E (VE)-coated dialyzer (n=15), or ERW treatment (n=15) during an HD course. The patients showed marked increases (15-fold) in blood reactive oxygen species, mostly H2O2, after HD without any treatment. HD resulted in decreased plasma VC, total antioxidant status, and erythrocyte metHb/ferricyanide reductase activity and increased erythrocyte levels of phosphatidylcholine hydroperoxide (PCOOH) and plasma metHb. Antioxidants treatment significantly palliated single HD course-induced oxidative stress, plasma and RBC PCOOH, and plasma metHb levels, and preserved erythrocyte metHb /ferricyanide reductase activity in an order VC>ERW>VE-coated dialyzer. However, ERW had no side effects of oxalate accumulation easily induced by VC. Six-month ERW treatment increased hematocrit and attenuated proinflammatory cytokines profile in the HD patients. In conclusion, ERW treatment administration is effective in palliating HD-evoked oxidative stress, as indicated by lipid peroxidation, hemolysis, and overexpression of proinflammatory cytokines in HD patients. Chronic hemodialysis (HD) patients increase erythrocyte susceptibility to hemolysis and impair cell survival. We explored whether electrolyte-reduced water (ERW) could palliate HD-evoked erythrocyte impairment and anemia. Forty-three patients undergoing chronic HD were enrolled and received ERW administration for 6 month. We evaluated oxidative stress in blood and plasma, erythrocyte methemoglobin (metHb)/ferricyanide reductase activity, plasma metHb, and proinflammatory cytokines in the chronic HD patients without treatment (n=15) or with vitamin C (VC)- (n=15), vitamin E (VE)-coated dialyzer (n=15), or ERW treatment (n=15) during an HD course. The patients showed marked increases (15-fold) in blood reactive oxygen species, mostly H2O2, after HD without any treatment. HD resulted in decreased plasma VC, total antioxidant status, and erythrocyte metHb/ferricyanide reductase activity and increased erythrocyte levels of phosphatidylcholine hydroperoxide (PCOOH) and plasma metHb. Antioxidants treatment significantly palliated single HD course-induced oxidative stress, plasma and RBC PCOOH, and plasma metHb levels, and preserved erythrocyte metHb /ferricyanide reductase activity in an order VC>ERW>VE-coated dialyzer. However, ERW had no side effects of oxalate accumulation easily induced by VC. Six-month ERW treatment increased hematocrit and attenuated proinflammatory cytokines profile in the HD patients. In conclusion, ERW treatment administration is effective in palliating HD-evoked oxidative stress, as indicated by lipid peroxidation, hemolysis, and overexpression of proinflammatory cytokines in HD patients. In patients undergoing hemodialysis (HD), the interaction of blood with non-biological materials of the extracorporeal circuit can activate polymorphonuclear leukocytes to produce quantities of reactive oxygen species (ROS), which impair neighboring tissues/cells (including RBCs) and evoke an inflammatory response.1.Sela S. Shurtz-Swirskin R. Shapiro G. et al.Oxidative stress during hemodialysis: effect of heparin.Kidney Int. 2001; 59: S159-S163Abstract Full Text PDF Scopus (50) Google Scholar, 2.Himmelfarb J. Lazaus J.M. Hakim R.M. Reactive oxygen species production by monocytes and polymorphonuclear leukocytes during hemodialysis.Am J Kidney Dis. 1991; 7: 271-276Abstract Full Text PDF Scopus (167) Google Scholar, 3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar The plasma levels of proinflammatory cytokines (e.g., interleukin (IL)-1, IL-6, tumor necrosis factor-α, and C-reactive protein) are significantly elevated in uremic patients on dialysis,3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 5.Descamps-Letscha B. Herbelin A. Nguyen A.T. et al.Balance between IL-1 beta, TNF-alpha, and their specific inhibitors in chronic renal failure and maintenance dialysis. Relationships with activation markers of T cells, B cells, and monocytes.J Immunol. 1995; 154: 882-892PubMed Google Scholar and the expression can be augmented further even after a single HD session.3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 6.Herbelin A. Nguyen A.T. Zingraff J. et al.Influence of uremia and hemodialysis on circulating interleukin-1 and tumor necrosis factor alpha.Kidney Int. 1990; 37: 116-125Abstract Full Text PDF PubMed Scopus (308) Google Scholar Increased oxidative stress and proinflammatory cytokines in HD patients are related to malnutrition,7.Danielski M. Ikizler T.A. mcMongale E. et al.Linkage of hypoalbuminemmia, inflammation, and oxidative stress in patients receiving maintenance hemodialysis therapy.Am J Kidney Dis. 2003; 42: 286-294Abstract Full Text Full Text PDF PubMed Scopus (136) Google Scholar resistance to erythropoietin therapy,8.Macdougall I.C. Could anti-inflammatory cytokine therapy improve poor treatment outcomes in dialysis patients?.Nephrol Dial Transplant. 2004; 19: V73-V78Crossref PubMed Scopus (30) Google Scholar cardiovascular events,9.Muller C. Eisenbrand G. Gradinger M. et al.Effects of hemodialysis, dialyser type and iron infusion on oxidative stress in uremic patients.Free Radic Res. 2004; 38: 1093-1100Crossref PubMed Scopus (48) Google Scholar, 10.Wratten M.L. Galaris D. Tetta C. Sevanian A. Evolution of oxidative stress and inflammation during hemodialysis and their contribution to cardiovascular disease.Antioxid Redox Signal. 2002; 4: 935-944Crossref PubMed Scopus (37) Google Scholar and high mortality.11.Zimmermann J. Herrlinger S. Pruy A. et al.Inflammation enhances cardiovascular risk and mortality in hemodialysis patients.Kidney Int. 1999; 55: 648-658Abstract Full Text Full Text PDF PubMed Scopus (1354) Google Scholar There is increasing evidence that oxidative stress plays a key role in the genesis and severity of dialysis anemia.12.Giardini O. Taccone-Gallucci M. Lubrano R. et al.Evidence of red blood cell membrane lipid peroxidation in hemodialysis patients.Nephron. 1984; 36: 235-237Crossref PubMed Scopus (105) Google Scholar, 13.Costagliola C. Romano L. Scibelli G. et al.Anemia and chronic renal failure: a therapeutical approach by reduced glutathione parenteral administration.Nephron. 1992; 61: 404-408Crossref PubMed Scopus (21) Google Scholar, 14.Canestrari F. Galli F. Giorgioni A. et al.Erytrocyte redox state in uremic anemia: effect of hemodialysis and relevance of glutathione metabolism.Acta Haematol. 1994; 91: 71-220Crossref Scopus (80) Google Scholar It reduces RBC survival,15.Usberti M. Lima G. Arisi M. et al.Effect of exogenous reduced glutathione on the survival of red blood cells in hemodialyzed patients.J Nephrol. 1997; 10: 261-265PubMed Google Scholar impairs the effect of erythropoietin,16.Cristol J.P. Bosh J.Y. Badiou S. et al.Erythropoietin and oxidative stress in hemodialysis. Beneficial effects of vitamin E supplementation.Nephrol Dial Transplant. 1997; 12: 2312-2317Crossref PubMed Scopus (157) Google Scholar, 17.Taccone-Gallucci M. Lubrano R. Meloni C. et al.Red blood cell membrane lipid peroxidation and resistance to erythropoietin therapy in hemodialyzed patients.Clin Nephrol. 1999; 52: 239-245PubMed Google Scholar and increases the susceptibility to hemolysis owing to inflammatory, infectious, and mechanical stimuli.13.Costagliola C. Romano L. Scibelli G. et al.Anemia and chronic renal failure: a therapeutical approach by reduced glutathione parenteral administration.Nephron. 1992; 61: 404-408Crossref PubMed Scopus (21) Google Scholar, 18.Galli F. Canestrari F. Buoncristiani U. Biological effects of oxidative stress in hemodialysis: the possible roles of vitamin E.Blood Purif. 1999; 17: 79-94Crossref PubMed Scopus (62) Google Scholar During the process of oxidative stress, RBCs are subject to membrane lipid peroxidation and susceptible to destruction.19.Weiss S.J. Neutrophil-mediated methemoglobin formation in the erythrocyte. The role of superoxide and hydrogen peroxide.J Biol Chem. 1982; 257: 2947-2953Abstract Full Text PDF PubMed Google Scholar, 20.Claster S. Chiu D.T. Quintanilha A. et al.Neutrophils mediate lipid peroxidation in human red cells.Blood. 1984; 64: 1079-1084Crossref PubMed Google Scholar, 21.Calo L.A. Stanic L. Davis P.A. et al.Effect of epoietin on HO-1 mRNA level and plasma antioxidants in hemodialysis patients.Int J Clin Pharmacol Ther. 2003; 41: 187-192Crossref PubMed Scopus (30) Google Scholar Increased ROS can oxidize oxyhemoglobin to yield H2O2 and methemoglobin (metHb)22.Kawanishi S. Caughey W.S. Mechanism of electron transfer to coordinated dioxygen of oxyhemoglobins to yield peroxide and methemoglobin. Protein control of electron donation by aquopentacyanoferrate(II).J Biol Chem. 1985; 260: 4622-4631Abstract Full Text PDF PubMed Google Scholar, 23.McLeod L.L. Alayash A.I. Detection of a ferrylhemoglobin intermediate in an endothelial cell model after hypoxia–reoxygenation.Am J Physiol Heart Circ Physiol. 1999; 46: H92-H99Google Scholar that, in turn, leads to tissue hypoxia,24.Zenser T.V. Lakshmi V.M. Hsu F.F. Davis B.B. Methemoglobin oxidation of N-acetylbenzidine to form a sulfinamide.Drug Metab Dispos. 2001; 29: 401-406PubMed Google Scholar endothelial cell G2/M arrest, and apoptosis.25.D'Agnillo F. Alayash A.I. Redox cycling of diaspirin cross-linked hemoglobin induces G2/M arrest and apoptosis in cultured endothelial cells.Blood. 2001; 98: 3315-3323Crossref PubMed Scopus (71) Google Scholar Increased H2O2 repressed metHb reductase expression in HeLa cells;26.Bello R.I. Alcain F.J. Gomez-Diaz C. et al.Hydrogen peroxide- and cell-density-regulated expression of NADH-cytochrome b5 reductase in HeLa cells.J Bioenerg Biomembr. 2003; 35: 169-179Crossref PubMed Scopus (29) Google Scholar deficiency of the enzyme, an autosomal recessive trait, results in hereditary methemoglobinemia (hemolysis).27.Dekker J. Eppink M.H. van Zwieten R. et al.Seven new mutations in the nicotinamide adenine dinucleotide reduced-cytochrome b(5) reductase gene leading to methemoglobinemia type I.Blood. 2001; 97: 1106-1114Crossref PubMed Scopus (49) Google Scholar A trans-plasma membrane electron transport system (e.g., nicotinamide adenine dinucleotide (reduced form)-ferricyanide reductase and NADH-metHb reductase) is present on RBC membranes and plays a role to reduce cytotoxic ferricyanide/metHb to functional ferrocyanide/oxyhemoglobin.28.Orringer E.P. Roer M.E.S. An ascorbate-mediated transmembrane-reducing system of the human erythrocyte.J Clin Invest. 1979; 63: 53-58Crossref PubMed Scopus (110) Google Scholar, 29.Borgese N. Pietrini G. gaetani S. Concentration of NADH-cytochrome b5 reductase in erythrocytes of normal and methemoglobinemic individuals measured with a quantitative radioimmunoblotting assay.J Clin Invest. 1987; 80: 1296-1302Crossref PubMed Scopus (21) Google Scholar Intravenous vitamin C (VC)- or vitamin E (VE)-coated dialyzer can improve HD-enhanced erythrocyte lipid peroxidation and hemolysis via the preservation of NADH-ferricyanide reductase and NADH-metHb reductase.4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar Electrolyte-reduced water (ERW) obtained by electrolysis scavenges O2-•, H2O2, and HOCl,3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 30.Shirahata S. Kabayama S. Nakano M. et al.Electrolyzed-reduced water scavenges active oxygen species and protects DNA from oxidative damage.Biochem Biophysic Res Commun. 1997; 234: 269-274Crossref PubMed Scopus (155) Google Scholar and protects DNA from oxidative damage.30.Shirahata S. Kabayama S. Nakano M. et al.Electrolyzed-reduced water scavenges active oxygen species and protects DNA from oxidative damage.Biochem Biophysic Res Commun. 1997; 234: 269-274Crossref PubMed Scopus (155) Google Scholar The protective mechanism of ERW results from active atomic hydrogen with high reducing ability, which can contribute to ROS-scavenging activity, and may participate in the redox regulation of cellular function.30.Shirahata S. Kabayama S. Nakano M. et al.Electrolyzed-reduced water scavenges active oxygen species and protects DNA from oxidative damage.Biochem Biophysic Res Commun. 1997; 234: 269-274Crossref PubMed Scopus (155) Google Scholar Active hydrogen in ERW may be an ideal scavenger against ROS because it does not produce oxidized molecules after reduction like other organic antioxidants (VC, VE, and polyphenols).31.Li Y. Nishimura T. Teruya K. et al.Protective mechanism of reduced water against alloxan-induced pancreatic cell damage: scavenging effect against reactive oxygen species.Cytotechnology. 2002; 40: 139-149Crossref PubMed Scopus (45) Google Scholar Our previous data reported that ERW administration diminished HD-enhanced H2O2 and HOCl activity, minimized atherosclerotic, oxidized and inflammatory markers, and partly restored total antioxidant status (TAS) during 1-month treatment.3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar In this study, 6 monthd of HD session was used in this study as in vivo system to evaluate the effects of ERW on dialysis-induced oxidative stress as indicated by erythrocyte lipid peroxidation, erythrocyte reductase activity, and metHb (hemolysis) levels. We also examined the long-term outcome of ERW on hematocrit, erythropoietin dose, and proinflammatory cytokine profiles in patients with end-stage renal disease (ESRD). An average 15-fold increase in blood ROS activity was noted in patients who underwent HD without ERW treatment. Replacement of ERW could effectively suppress the ROS formation by 75±14% in HD patients (Figure 1a). VC- or VE-coated dialyzer inhibited HD-enhanced ROS by 83±11 or 49±9%. Post-HD blood samples obtained from the group were used for examining the effects of several antioxidants. The augmented blood ROS counts were greatly inhibited by an H2O2 scavenger, catalase (by 68±8%), and partially depressed by superoxide dismutase (14±5%) and epigallocatechin-3-gallate (16±5%) (Figure 1b), indicating that the majority of the blood ROS activity was derived from H2O2. ERW depressed ROS activity by 60±8%. In the XERW group, the post-HD plasma VC and TAS levels were significantly decreased (Figure 2). This indicates that HD can cause acute oxidative stress and acute loss of plasma VC. In the VC group, intravenous VC significantly (P<0.05) increased the plasma VC and TAS levels in ESRD patients receiving HD. Patients for whom the VE-coated dialyzer was used did not seem to have restored plasma VC and TAS levels. ERW treatment could restore plasma VC and TAS levels. In all four groups, there was no significant change in plasma VE and oxalate concentrations. However, an increased tendency of oxalate concentration was found in the VC group, suggesting a possibly adverse side effect of long-term intravenous VC. In our previous studies,3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar a single session of HD did not affect the levels of lipid profiles in the ESRD patients. The baseline level of pre-HD plasma phosphatidylcholine hydroperoxide (PCOOH) and erythrocyte membrane PCOOH was similar among the four groups of patients. However, in the XERW group, the post-HD plasma PCOOH (205±24 pmol/ml) and post-HD erythrocyte membrane PCOOH levels (310±39 pmol/ml) were significantly (P<0.05) increased after HD (Figure 3). Intravenous VC significantly (P<0.05) prevented increases in post-HD plasma PCOOH (110±15 pmol/ml) and in post-HD RBC membrane PCOOH levels (168±25 pmol/ml). In the VE group, the VE-coated dialyzer also decreased the increase in post-HD plasma PCOOH level (145±21 pmol/ml, P<0.05). On the other hand, the VE-coated dialyzer also prevented the increase in post-HD RBC membrane PCOOH levels (178±29 pmol/ml, P<0.05). In the ERW group, ERW treatment significantly reduced post-HD plasma PCOOH (134±18 pmol/ml, P<0.05) and post-HD RBC membrane PCOOH levels (163±19 pmol/ml, P<0.05). A single session of HD inhibited the activities of NADH- metHb reductase and NADH-ferricyanide reductase in erythrocytes, and it increased plasma metHb levels (Figure 4). Intravenous VC, VE, or ERW treatment significantly preserved the activities of erythrocyte ferricyanide reductase and erythrocyte metHb reductase, and decreased the HD-augmented metHb level. These findings imply that ERW treatment was effective in preventing oxidative stress on erythrocytes. To determine the long-term effects of ERW in the ESRD patients undergoing chronic HD, we recorded the post-HD blood ROS, post-HD levels of activities of NADH-metHb reductase and NADH-ferricyanide reductase in erythrocyte membrane, and post-HD plasma metHb level in the ERW- and XERW-treated patients for 6 months. As shown in Figure 5, after 6 months of ERW treatment in the ESRD patients with chronic HD, the increased post-HD blood ROS was decreased (P<0.05) when compared to XERW group, whereas the post-HD levels of activities of NADH-metHb reductase and NADH-ferricyanide reductase were increased (P<0.05) when compared to the XERW group. The post-HD plasma metHb level was also significantly decreased (P<0.05) in the ERW group when compared to the XERW group. The long-term outcome showed that 6-month ERW treatment significantly increased hematocrit (from 28.9±0.7 to 31.5±0.6%) at a similar dose of erythropoietin administration in the 43 chronic HD patients (Figure 6). However, the differences of hematocrit change were not statistically significant in the XERW group (from 31.0±1.0 to 30.7±0.4%) even at a similar dose of erythropoietin. Furthermore, after 6 months of ERW treatment, 26 plasma cytokines critical to the inflammatory response are also downregulated (Figure 7).Figure 6Effects of 6-month ERW treatment on post-HD-affected hematocrit (Hct) and erythropoietin dose (EPO) in 43 ESRD patients. Twenty-five ESRD patients without ERW treatment (XERW) were used control group. M0, before ERW treatment; M1, ERW treatment for 1 month; M3, ERW treatment for 3 months; and M6, ERW treatment for 6 months.View Large Image Figure ViewerDownload (PPT)Figure 7Determination of multiple cytokines determination by cytokine antibody array in the pre-HD plasma of one ESRD patient before and during 6-month ERW treatment. (a) The pre-HD plasma cytokine profiles and (b) amplified dot plot of cytokines before, after 1-month (1 M), 3-month (3 M), and 6-month (6 M) ERW treatment are displayed. Note that ERW treatment significantly reduced the dot-spot intensity of proinflammatory cytokines (a–z) after 6 M of ERW treatment. a, insulin growth factor-1; b, IL-13; c, IL-15; d, IL-16; e, IL-1β; f, IL-1ra; g, IL-2; h, IL-6; I, membrane cofactor protein-2; j, membrane cofactor protein-3; k, membrane cofactor protein-4; l, macrophage-colony-stimulating factor; m, MDC; n, MIG; o, macrophage inflammatory protein-1δ; p, NAP-2; q, NT-3; r, platelet-derived growth factor-BB; s, RANTES; t, stem cell factor; u, SDF-1; v, TARC; w, tumor growth factor-β1; x, tumor growth factor-β3; y, tumor necrosis factor-α; z, tumor necrosis factor-β; -, negative dot; +, positive dot.View Large Image Figure ViewerDownload (PPT) Our study indicates that HD activated polymorphonuclear leukocytes and monocytes to release of ROS, mostly H2O23.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar and was accompanied by adverse events in ESRD patients, including (1) increased amount of ROS in the blood; (2) peroxidation of plasma lipid and RBC membrane lipid; (3) inhibition of the activity of erythrocyte reductases, leading to hemolysis. The application of ERW can decrease HD-enhanced blood ROS production, RBC lipid peroxidation, and hemolysis via the preservation of NADH-ferricyanide reductase and -metHb reductase activity. This beneficial long-term outcome of 6-month ERW treatment can improve the hematocrit without the increment of erythropoietin dosage. The oxidative stress associated with uremia is exacerbated by hemodialysis since neutrophils and monocytes, activated by contact with the dialysis membranes, release large amounts of ROS.1.Sela S. Shurtz-Swirskin R. Shapiro G. et al.Oxidative stress during hemodialysis: effect of heparin.Kidney Int. 2001; 59: S159-S163Abstract Full Text PDF Scopus (50) Google Scholar, 2.Himmelfarb J. Lazaus J.M. Hakim R.M. Reactive oxygen species production by monocytes and polymorphonuclear leukocytes during hemodialysis.Am J Kidney Dis. 1991; 7: 271-276Abstract Full Text PDF Scopus (167) Google Scholar, 3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar The deleterious effects of ROS on carbohydrates, lipids, and proteins have a pathological role in many inflammatory diseases, most of which are frequent in HD patients.5.Descamps-Letscha B. Herbelin A. Nguyen A.T. et al.Balance between IL-1 beta, TNF-alpha, and their specific inhibitors in chronic renal failure and maintenance dialysis. Relationships with activation markers of T cells, B cells, and monocytes.J Immunol. 1995; 154: 882-892PubMed Google Scholar, 12.Giardini O. Taccone-Gallucci M. Lubrano R. et al.Evidence of red blood cell membrane lipid peroxidation in hemodialysis patients.Nephron. 1984; 36: 235-237Crossref PubMed Scopus (105) Google Scholar In particular, the oxidation of polyunsaturated fatty acids on the RBC membrane3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar, 12.Giardini O. Taccone-Gallucci M. Lubrano R. et al.Evidence of red blood cell membrane lipid peroxidation in hemodialysis patients.Nephron. 1984; 36: 235-237Crossref PubMed Scopus (105) Google Scholar increases RBC rigidity and reduces their deformability,32.Pfafferott C. Neiselman J. Hochstein P. The effect of malonyldialdehyde on erythrocyte deformability.Blood. 1982; 59: 12-15Crossref PubMed Google Scholar, 33.Zachee P. Ferrant A. Daelemans R. et al.Oxidative injury to erythrocytes, cell rigidity and splenic hemolysis in hemodialyzed patients before and during erythropoietin treatment.Nephron. 1988; 65: 288-293Google Scholar leading to greater susceptibility to hemolysis,4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar and shorter survival.15.Usberti M. Lima G. Arisi M. et al.Effect of exogenous reduced glutathione on the survival of red blood cells in hemodialyzed patients.J Nephrol. 1997; 10: 261-265PubMed Google Scholar ROS may cause subsequent oxidation and release of other oxidized metabolites and are increased after HD session.3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar As a primary peroxidation product from membrane phospholipids, the level of PCOOH in the plasma and erythrocyte membrane was increased by HD.3.Huang K.C. Yang C.C. Lee K.T. Chien C.T. Reduced hemodialysis-induced oxidative stress in end-stage renal disease patients by electrolyzed reduced water.Kidney Int. 2003; 64: 704-714Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar, 4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar Further, the significant increases of metHb and the decreased activity of two RBC reductases (NADH-ferricyanide reductase and -metHb reductase) in post-HD plasma and RBC implicate potential RBC damage secondary to lipid peroxidation. Human oxyhemoglobin reacts with Fe(II)(CN)5H2O3- to yield H2O2 and metHb.22.Kawanishi S. Caughey W.S. Mechanism of electron transfer to coordinated dioxygen of oxyhemoglobins to yield peroxide and methemoglobin. Protein control of electron donation by aquopentacyanoferrate(II).J Biol Chem. 1985; 260: 4622-4631Abstract Full Text PDF PubMed Google Scholar Further, metHb production can be accelerated by H2O2.34.Winterbourn C.C. Oxidative reactions of hemoglobin.Methods Enzymol. 1990; 186: 265-272Crossref PubMed Scopus (385) Google Scholar In our previous study, HD-triggered H2O2 formation was positively correlated with the degree of hemolysis and with metHb levels.4.Yang C.C. Hsu S.P. Wu M.S. et al.Effects of vitamin C infusion and vitamin E-coated membrane on hemodialysis-induced oxidative stress.Kidney Int. 2006; 69: 706-714Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar Based upon the interesting clinical improvement of a variety of diseases by intake of reduced water since 1985, Hayashi35.Hayashi H. Water regulating theory: Hayashi's model.Explore. 1995; 6: 28-31Google Scholar proposed the hypothesis ‘Water Regulating Theory’. The ideal scavenger for ROS should be active atomic hydrogen. Active atomic hydrogen can be produced in ERW near the cathode during electrolysis of water. ERW exhibits high pH, low dissolved oxygen, extremely high dissolved molecular hydrogen, and extremely negative redox potential values.30.Shirahata S. Kabayama S. Nakano M. et al.Electrolyzed-reduced water scavenges active oxygen species and protects DNA from oxidative damage.Biochem Biophysic Res Commun. 1997; 234: 269-274Crossref PubMed Scopus (155) Google Scholar Shirahata et al.30.Shirahata S. Kabayama S. Nakano M. et al.Electrolyzed-reduced water scavenges active oxygen species and protects DNA from oxidative damage.Biochem Biophysic Res Commun. 1997; 234: 269-274Crossref PubMed Scopus (155) Google Scholar suggest that the superoxide dismutase- and catalase-like activity of ERW is not owing to the dissolved molecular hydrogen but owing to the active atomic hydrogen with a higher reducing ability that may participate in ROS-scavenging activity. Happe et al.36.Happe R.P. Roseboom W. Pierik A.J. et al.Biological activation of hydrogen.Nature. 1997; 385: 126Crossref PubMed Scopus (386) Google Sch" @default.
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• W2001993344 title "Electrolyzed-reduced water reduced hemodialysis-induced erythrocyte impairment in end-stage renal disease patients" @default.
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