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      Does Glucose Present in the Dialysate Limit Oxidative Stress in Patients Undergoing Regular Hemodialysis?

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          Background: Decreased glucose concentration in the blood causes the inhibition of the hexose monophosphate (HMP) cycle in the erythrocyte. NADPH, which is the source of the reductive equivalents necessary for the reproduction of glutathione (GSH), is not regenerated. The presence of glucose in dialysate should provide the stability of its concentration in the blood of patients undergoing hemodialysis (HD). The aim of the study was to assess the influence of glucose in the dialysate on the intensity of oxidative stress in patients undergoing regular HD. Methods: The study comprised 43 patients hemodialyzed with dialysate containing (HD-g(+)) or not containing glucose (HD-g(–)). The concentrations of the products of reaction with thiobarbituric acid-reactive substance (TBARS) and GSH as well as the activity of erythrocyte superoxide dismutase were determined. Glucose concentrations in the blood before and immediately after dialysis were also measured. Results: After flow-through dialysis the glucose concentration in the blood decreases both when dialysate does not contain glucose (4.8 vs. 1.6 mmol/l) and when dialysate contains glucose (6.6 vs. 5.8 mmol/l). HD caused changes in the TBARS concentration: in the HD-g(+) group the concentration decreased after HD, whereas in the HD-g(–) group it increased. In both groups of patients studied the GSH concentration changed after HD; in the HD-g(–) group it decreased and in the HD-g(+) group it increased. The results obtained in the groups of patients examined were confirmed by in vitro studies. Conclusions: The presence of glucose in the dialysate guarantees the normal activity of the HMP cycle, which provides the production of reductive equivalents for the regeneration of reduced GSH – free radicals scavenger – and therefore the limitation of oxidative stress.

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          Most cited references 13

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          Oxidative stress at onset and in early stages of type 1 diabetes in children and adolescents.

          In diabetes, the persistence of hyperglycemia has been reported to cause increased production of oxygen free radicals through glucose autooxidation and nonenzymatic glycation. The aim of this study was to determine whether oxidative cellular damage occurs at the clinical onset of diabetes and in later stages of the disease in young patients. Indicative parameters of lipoperoxidation, protein oxidation, and changes in the status of antioxidant defense systems were evaluated in single blood samples from 54 diabetic children, adolescents, and young adults and 60 healthy age- and sex-matched control subjects. Malondialdehyde and protein carbonyl group levels in plasma were progressively higher in diabetic children and adolescents than in control subjects (P < 0.0001). The highest erythrocyte superoxide dismutase (SOD) activity was found in diabetic children at onset of clinical diabetes. In diabetic adolescents, SOD was also significantly higher (P < 0.0001) than in control subjects. Erythrocyte glutathione peroxidase was significantly lower in diabetic children and adolescents compared with control subjects (P < 0.002). A significant decline in blood glutathione content at the recent onset of diabetes was found (P < 0.0001). Furthermore, our results demonstrated progressive glutathione depletion during diabetes evolution. The plasma alpha-tocopherol/total lipids ratio and beta-carotene levels during diabetes development (P < 0.001) were low. This cross-sectional study in young diabetic patients showed that systemic oxidative stress is present upon early onset of type 1 diabetes and is increased by early adulthood. Decreased antioxidant defenses may increase the susceptibility of diabetic patients to oxidative injury. Appropriate support for enhancing antioxidant supply in these young diabetic patients may help prevent clinical complications during the course of the disease.
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            Oxidative stress and haemodialysis: role of inflammation and duration of dialysis treatment.

            Oxidative stress has long been demonstrated in haemodialysis patients. However, the factors influencing their oxidative status have not been characterized extensively in these patients. Therefore, the present study was designed to investigate the influence of a large number of factors known to be associated with oxidative stress. In the present cross-sectional study, we determined the plasma levels of lipid and protein oxidation markers in 31 non-smoking haemodialysis patients and 18 non-smoking healthy subjects, together with various components of the antioxidant system at the plasma and erythrocyte level. No influence of age, diabetes or iron overload on oxidative markers and plasma and erythrocyte antioxidant systems was detected in these haemodialysis patients. The lack of an association between iron overload and oxidative status may be related to the lower level of plasma ascorbate in haemodialysis patients, since ascorbate favours the generation of free iron from ferritin-bound iron. Interestingly, plasma C reactive protein (CRP) levels measured by highly sensitive CRP assay were correlated positively with plasma levels of thiobarbituric acid reactive substances (r=0.38, P<0.04) and negatively with plasma alpha-tocopherol levels (r=-0.46, P<0.01). Moreover, significant inverse correlations were observed between duration of dialysis treatment and plasma levels of alpha-tocopherol (r=-0.49, P<0.02) and ubiquinol (r=-0.40, P<0.05). Our results suggest that inflammatory status and duration of dialysis treatment are the most important factors relating to oxidative stress in haemodialysis patients.
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              Glutathione antioxidant system as a marker of oxidative stress in chronic renal failure


                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                May 2005
                19 May 2005
                : 23
                : 3
                : 219-225
                Departments of aChemistry and Biochemistry, and bNephrology, Transplantology and Internal Medicine, Pomeranian Medical University, Szczecin, Poland
                84906 Blood Purif 2005;23:219–225
                © 2005 S. Karger AG, Basel

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                Figures: 4, Tables: 2, References: 26, Pages: 7
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