ArticleClinical and experimental nephrology2005
Glutathione peroxidase activity in patients with renal disorders.
Article in Clinical and experimental nephrology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 59 citations in OpenAlex.
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- Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
- The Role of Eryptosis in the Pathogenesis of Renal Anemia: Insights From Basic Research and Mathematical Modeling.Frontiers in cell and developmental biology · 2020Review
- Delta-Aminolevulinate dehydratase and glutathione peroxidase activity in Alzheimer's disease: a case-control study.EXCLI journal · 2019Article
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- Effects of resveratrol on hydrogen peroxide-induced oxidative stress in embryonic neural stem cells.Neural regeneration research · 2013Article
- Serum malondialdehyde levels, myeloperoxidase and catalase activities in patients with nephrotic syndrome.Redox report : communications in free radical research · 2013Observational
- Oxidant/antioxidant status and hyperfiltration in young patients with type 1 diabetes mellitus.Pediatric nephrology (Berlin, Germany) · 2009Article
- Plasma and erythrocyte glutathione peroxidase activity, serum selenium concentration, and plasma total antioxidant capacity in cats with IRIS stages I-IV chronic kidney disease.Journal of veterinary internal medicineArticle
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundGlutathione peroxidase (GPx) protects cells from oxidative damage by catalyzing the reduction of both organic and hydrogen peroxides, using glutathione as a reducing agent. Both plasma GPx (P-GPx) and erythrocyte GPx (E-GPx) have been identified in human blood. Kidney proximal tubular cells are the main source of GPx activity in the plasma. Oxidative damage has been reported to participate in the progression and complications of renal diseases.
methodsThe activities of both E-GPx and P-GPx were determined, using Randox commercial kits, in 12 patients with nephrotic syndrome (NS), 48 patients with renal impairment (RI), and 50 patients with chronic renal failure on maintenance hemodialysis (HD; before as well as immediately after dialysis), and in 50 healthy volunteers who served as controls.
resultsCompared to the results in healthy controls, P-GPx activity was reduced in the HD group and the RI group, whereas the NS group showed no significant difference from the control. The HD group showed a higher drop in P-GPx (reduced to 36.6% of the mean control value) than the RI group (reduced to 61.8% of the mean control value). Further analysis of the RI group showed a highly significant negative correlation between P-GPx activity and serum creatinine level (r = -0.691; P < 0.001). Also, a highly significant negative correlation was found between P-GPx and blood urea nitrogen (r = -0.792; P < 0.001). However, E-GPx activity showed no significant correlation with either serum creatinine or blood urea nitrogen. E-GPx was reduced to 55.2% and 68.9% of the mean control 1 value in the NS group and the RI group respectively, while the HD group showed no significant change. Further analysis of the RI group found that E-GPx activity showed no significant correlation with either serum creatinine or blood urea nitrogen. In HD patients, GPx activity was measured before and immediately after hemodialysis. E-GPx activity was similar before and after dialysis, without a significant difference (pre-dialysis, 37.7 +/- 13.5 U/g hemoglobin [Hb]; post-dialysis, 38.72 +/- 12.31 U/g Hb). However, P-GPx activity was significantly increased (pre-dialysis, 254.4 +/- 62.6 U/ml; post-dialysis, 296.98 +/- 74.04 U/ml; P < 0.001), but it was still significantly lower when compared to that in the healthy controls.
conclusionsP-GPx activity is an important test to assess the oxidative damage in patients with kidney diseases. The progression of renal disorders is accompanied by a decrease in P-GPx activity, but not by a decrease in E-GPx activity. Thus, we conclude that P-GPx activity largely depends on physiological renal function, whereas E-GPx activity does not.
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