title: Oxidative stress and antioxidant defense mechanism in glomerular diseases.
abstract: The changes in red blood cell (RBC) lipid peroxidation [measured via the malonyl dialdehyde (MDA) concentration], reduced (GSH), and oxidized glutathione (GSSG) levels, hemoglobin (Hb) oxidation and antioxidant enzyme [catalase (Cat), glutathione peroxidase, and superoxide dismutase (SOD)] activities were studied in 45 pediatric patients with various glomerular diseases [minimal change nephrotic syndrome (MCNS) in relapse or in remission, lupus nephropathy (SLE), poststreptococcal glomerulonephritis (APSGN), IgA nephropathy (IGA gn)], and in 20 adult patients with IGA gn and also in 15 pediatric and 14 adult controls. The in vitro effects of hydrogen peroxide [acetyl phenylhydrazine (APH) test] on the GSH and Hb metabolisms were likewise investigated. There was an increased oxidative stress in MCNS with relapse, IGA gn, SLE gn, and APSGN, which could be detected in the GSH and Hb oxidation and in the lipid peroxidation on the peripheral RBC-s. The RBC SOD and Cat activities were significantly lower in all patients than in the controls. The RBC GSSG level was significantly elevated in all patients, with the exception of MCNS in remission. This stimulated a compensatory GSH production in MCNS with relapse and in IGA gn, but not in SLE or APSGN. The regeneration of GSH from GSSG was reduced in MCNS with relapse, SLE, and IGA gn, but not in APSGN. In remission, the GSH-GSSG redox system normalizes, but in vitro the APH test stimulates an intensive Hb oxidation. In conclusion, there is a correlation between the presence of active glomerular disease and the evidence of oxidative changes in the various parameters measured in peripheral RBCs.
authors.affiliation: Department of Paediatrics, Albert Szent-Györgyi Medical University, Szeged, Hungary.
authors.forename: S
authors.initials: S
authors.lastname: Túri
authors.forename: I
authors.initials: I
authors.lastname: Németh
authors.forename: A
authors.initials: A
authors.lastname: Torkos
authors.forename: L
authors.initials: L
authors.lastname: Sághy
authors.forename: I
authors.initials: I
authors.lastname: Varga
authors.forename: B
authors.initials: B
authors.lastname: Matkovics
authors.forename: J
authors.initials: J
authors.lastname: Nagy
mesh_terms: D000293:Adolescent; D000328:Adult; D000975:Antioxidants / Q000378:metabolism*; D016022:Case-Control Studies; D002374:Catalase / Q000097:blood; D002648:Child; D002675:Child, Preschool; D004912:Erythrocytes / Q000201:enzymology / Q000378:metabolism*; D005260:Female; D005921:Glomerulonephritis / Q000097:blood / Q000503:physiopathology*; D005978:Glutathione / Q000031:analogs & derivatives / Q000097:blood; D019803:Glutathione Disulfide; D005979:Glutathione Peroxidase / Q000097:blood; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D009402:Nephrosis, Lipoid / Q000097:blood / Q000503:physiopathology*; D018384:Oxidative Stress / Q000502:physiology*; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: D000975:Antioxidants; D006454:Hemoglobins; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D019803:Glutathione Disulfide