Otmail.com; Rogelio Hern dezPando – [email protected]; Norma A Mac s-Ruvalcaba – [email protected]; Perla D Maldonado – [email protected]; Marcos I Salcedo – [email protected]; Edilia Tapia – [email protected]; Liliana Sald ar – [email protected]; Mar E Castilla – [email protected]; Mar E Ibarra-Rubio – [email protected] * Corresponding authorTime course study of oxidative and nitrosative stress and antioxidant enzymes in K2Cr2O7-induced nephrotoxicityPublished: 26 April 2005 BMC Nephrology 2005, 6:4 doi:10.1186/1471-2369-6-Received: 30 October 2004 Accepted: 26 AprilThis article is available from: http://www.biomedcentral.com/1471-2369/6/4 ?2005 Pedraza-Chaverr?et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractBackground: 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–D-glucosaminidase (NAG) and total protein. Oxidative and nitrosative stress were measured by immunohistochemical localization of protein BIM-22493 site carbonyls and 3nitrotyrosine, 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?) and by the increase in serum creatinine (days 1?), BUN (days 1?), urinary excretion of NAG (days 1?), andPage 1 of(page number not for citation purposes)BMC Nephrology 2005, 6:http://www.biomedcentral.com/1471-2369/6/total protein (day 1?) and by the structural damage to the proximal tubules (days 1?). Oxidative and nitrosative stress were clearly evident on days 1?. Urinary excretion of NO2-/NO3- decreased on days 2?. Mn-SOD and Cu, Zn-SOD, estimated by immunohistochemistry, and total SOD activity remained unchanged. Activity of GPx decreased on days 3?2 and those of GR and CAT on days 2?0. 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 PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27735993 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 stres.