Time course study of oxidative and nitrosative stress and antioxidant enzymes in K2Cr2O7-induced nephrotoxicity
| Autor: | José Pedraza-Chaverri, Rogelio Hernández-Pando, Marcos I Salcedo, Norma A. Macías-Ruvalcaba, Raymundo C Carvajal, Edilia Tapia, Diana Barrera, Liliana Saldívar, María Elena Ibarra-Rubio, Omar Noel Medina-Campos, Perla D. Maldonado, María E Castilla |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2005 |
| Předmět: |
Chromium
Male medicine.medical_specialty Antioxidant medicine.medical_treatment Glutathione reductase Oxidative phosphorylation Pharmacology medicine.disease_cause lcsh:RC870-923 Kidney Nephrotoxicity Superoxide dismutase Kidney Tubules Proximal Internal medicine Acetylglucosaminidase medicine Animals Rats Wistar Nitrogen Compounds Nitrites chemistry.chemical_classification Glutathione Peroxidase Nitrates biology business.industry Superoxide Dismutase Glutathione peroxidase lcsh:Diseases of the genitourinary system. Urology Catalase Creatine Immunohistochemistry Rats Oxidative Stress Proteinuria chemistry Nephrology biology.protein Kidney Diseases Potassium Dichromate business Oxidoreductases Oxidative stress Research Article |
| Zdroj: | BMC Nephrology BMC Nephrology, Vol 6, Iss 1, p 4 (2005) |
| ISSN: | 1471-2369 |
| Popis: | Background Potassium dichromate (K2Cr2O7)-induced nephrotoxicity is associated with oxidative and nitrosative stress. In this study we investigated the relation between the time course of the oxidative and nitrosative stress with kidney damage and alterations in the following antioxidant enzymes: Cu, Zn superoxide dismutase (Cu, Zn-SOD), Mn-SOD, glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT). Methods Nephrotoxicity was induced in rats by a single injection of K2Cr2O7. Groups of animals were sacrificed on days 1,2,3,4,6,8,10, and 12. Nephrotoxicity was evaluated by histological studies and by measuring creatinine clearance, serum creatinine, blood urea nitrogen (BUN), and urinary excretion of N-acetyl-β-D-glucosaminidase (NAG) and total protein. Oxidative and nitrosative stress were measured by immunohistochemical localization of protein carbonyls and 3-nitrotyrosine, respectively. Cu, Zn-SOD, Mn-SOD, and CAT were studied by immunohistochemical localization. The activity of total SOD, CAT, GPx, and GR was also measured as well as serum and kidney content of chromium and urinary excretion of NO2 -/NO3-. Data were compared by two-way analysis of variance followed by a post hoc test. Results Serum and kidney chromium content increased reaching the highest value on day 1. Nephrotoxicity was made evident by the decrease in creatinine clearance (days 1–4) and by the increase in serum creatinine (days 1–4), BUN (days 1–6), urinary excretion of NAG (days 1–4), and total protein (day 1–6) and by the structural damage to the proximal tubules (days 1–6). Oxidative and nitrosative stress were clearly evident on days 1–8. Urinary excretion of NO2-/NO3- decreased on days 2–6. Mn-SOD and Cu, Zn-SOD, estimated by immunohistochemistry, and total SOD activity remained unchanged. Activity of GPx decreased on days 3–12 and those of GR and CAT on days 2–10. Similar findings were observed by immunohistochemistry of CAT. Conclusion These data show the association between oxidative and nitrosative stress with functional and structural renal damage induced by K2Cr2O7. Renal antioxidant enzymes were regulated differentially and were not closely associated with oxidative or nitrosative stress or with kidney damage. In addition, the decrease in the urinary excretion of NO2-/NO3- was associated with the renal nitrosative stress suggesting that nitric oxide was derived to the formation of reactive nitrogen species involved in protein nitration. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink