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      Vitamins A, E and C as Non-Enzymatic Antioxidants and Their Relation to Lipid Peroxidation in Children with Chronic Renal Failure

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          Background: Increased lipid peroxidation (LP) and reduced enzymatic antioxidant defense have been observed in predialysis patients with advanced chronic renal failure (CRF) and in patients on maintenance hemodialysis (HD). To extend these observations, we evaluated the plasma, erythrocyte and dialysate levels of vitamins A and E and the plasma and dialysate levels of vitamin C as exogenous non-enzymatic antioxidants in children with CRF treated conservatively and on HD. The data obtained were related to LP monitored by erythrocyte malonyldialdehyde (E-MDA) and plasma organic hydroperoxide (OHP) concentrations. Patients: Forty-six predialysis children were enrolled in the study and divided into 2 groups: group I = moderate CRF (plasma creatinine <265.3 µmol/l), and group II = plasma creatinine ≧265.3 µmol/l. Group III consisted of 21 HD children. 27 age-matched healthy subjects served as a control group. Results: The plasma levels of vitamin A and vitamin C were significantly reduced in all CRF patients when compared to the controls, with the lowest values observed in children on maintenance HD (group III). Significant differences were also noted between the moderate CRF (group I) and HD (group III). Plasma levels of vitamin E were significantly decreased in moderate CRF (group I) and HD (group III) as compared to controls. In contrast, the erythrocyte vitamin A and vitamin E levels of predialysis children and HD patients were not different from the controls. The E-MDA and OHP concentrations in the 3 groups of CRF children were significantly higher than in healthy subjects. The concentration of plasma vitamin C was significantly inversely correlated with E-MDA, plasma OHP and creatinine in group I. In group II we found a significant correlation of plasma vitamin E levels with creatinine and E-MDA and a correlation of the plasma vitamin C concentration with E-MDA. Conclusion: CRF in children is associated with decreased concentrations of plasma antioxidant vitamins. This reduction is most expressed in children on maintenance HD and particularly concerns plasma vitamin C and erythrocyte vitamin E concentrations. The low levels of plasma vitamin A, E and C might result in reduced activity of the non-enzymatic antioxidant defense system and might be responsible for increased oxidative stress occurring in children with CRF.

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          Most cited references 26

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          Secondary prevention with antioxidants of cardiovascular disease in endstage renal disease (SPACE): randomised placebo-controlled trial

           U Gafter,  A Iaina,  A. Knecht (2000)
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            Oxidative stress and dysregulation of superoxide dismutase and NADPH oxidase in renal insufficiency.

            Chronic renal failure (CRF) is associated with oxidative stress, the mechanism of which remains uncertain. Superoxide is the primary oxygen free radical produced in the body, NAD(P)H oxidase is the major source of superoxide production and superoxide dismutase (SOD) is responsible for removal of superoxide. We hypothesized that CRF-induced oxidative stress may be due to increased production and/or decreased dismutation of superoxide. Immunodetectable superoxide dismutase isoforms (Cu Zn SOD and Mn SOD), as well as, NAD(P)H oxidase (gp91 phox subunit) proteins and xanthine oxidase (XO) activity were determined in the kidney and liver of CRF (5/6 nephrectomized) and sham-operated control rats. Subgroups of animals were treated with SOD-mimetic drug, tempol and blood pressure and urinary nitric oxide metabolites (NOx) were monitored. The CRF group showed marked down-regulations of CuZn SOD and Mn SOD and significant up-regulation of gp91 phox in the liver and kidney, which are among the metabolically most active tissues. In contrast, XO activity was depressed in both tissues. Arterial pressure and nitrotyrosine abundance were elevated while urinary NOx excretion was depressed, pointing to increased NO inactivation by superoxide and decreased NO availability in CRF animals. Administration of SOD-mimetic agent, tempol, for one week, ameliorated hypertension, reduced nitrotyrosine abundance and increased urinary NOx excretion in the CRF animals. CRF is associated with depressed SOD and elevated NAD(P)H oxidase expression, which can contribute to oxidative stress by increasing superoxide. This is evidenced by favorable response to administration of SOD-mimetic drug, tempol, and increased nitrotyrosine that is the footprint of NO interaction with superoxide.
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              Plasma protein thiol oxidation and carbonyl formation in chronic renal failure.

              Myeloperoxidase-catalyzed oxidative pathways have recently been identified as an important cause of oxidant stress in uremia and hemodialysis (HD), and can lead to plasma protein oxidation. We have examined patterns of plasma protein oxidation in vitro in response to hydrogen peroxide (H2O2) and hypochlorous acid (HOCl). We measured thiol oxidation, amine oxidation, and carbonyl concentrations in patients on chronic maintenance HD compared with patients with chronic renal failure (CRF) and normal volunteers. We have also examined the effect of the dialysis procedure on plasma protein oxidation using biocompatible and bioincompatible membranes. Plasma proteins were assayed for the level of free thiol groups using spectrophotometry, protein-associated carbonyl groups by enzyme-linked immunosorbent assay, and oxidation of free amine groups using a fluorescent spectrophotometer. In vitro experiments demonstrate HOCl oxidation of thiol groups and increased carbonyl formation. In vivo, there are significant differences in plasma-free thiol groups between normal volunteers (279 +/- 12 micromol/L), CRF patients (202 +/- 20 micromol/L, P = 0.005) and HD patients (178 +/- 18 micromol/L, P = 0.0001). There are also significant differences in plasma protein carbonyl groups between normal volunteers (0.76 +/- 0.51 micromol/L), CRF patients (13.73 +/- 4.45 micromol/L, P = 0.015), and HD patients (16.95 +/- 2.62 micromol/L, P = 0.0001). There are no significant differences in amine group oxidation. HD with both biocompatible and bioincompatible membranes restored plasma protein thiol groups to normal levels, while minimally affecting plasma protein carbonyl expression. First, both CRF and HD patients have increased plasma protein oxidation manifested by oxidation of thiol groups and formation of carbonyl groups. Second, HD with biocompatible and bioincompatible membranes restored plasma protein thiol groups to normal levels. Third, these experiments suggest that there is a dialyzable low molecular weight toxin found in uremia that is responsible for plasma protein oxidation.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                April 2006
                21 December 2005
                : 103
                : 1
                : c12-c18
                aDepartment of Pediatric Nephrology, Wrocław Medical University, Wrocław, bDepartment and Clinic of Internal Medicine, Diabetology and Nephrology, Silesian School of Medicine, Zabrze, and cDepartment of Pediatrics, Clinic of Pediatrics, Nephrology and Endocrinology of Childhood, Silesian School of Medicine, Zabrze, Poland
                90506 Nephron Clin Pract 2006;103:c12–c18
                © 2006 S. Karger AG, Basel

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                Tables: 4, References: 45, Pages: 1
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