Time course study of oxidative and nitrosative stress and antioxidant enzymes in K2Cr2O7-induced nephrotoxicity View Full Text


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Article Info

DATE

2005-04-26

AUTHORS

José Pedraza-Chaverrí, Diana Barrera, Omar N Medina-Campos, Raymundo C Carvajal, Rogelio Hernández-Pando, Norma A Macías-Ruvalcaba, Perla D Maldonado, Marcos I Salcedo, Edilia Tapia, Liliana Saldívar, María E Castilla, María E Ibarra-Rubio

ABSTRACT

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-beta-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. More... »

PAGES

4-4

References to SciGraph publications

  • 1992-11. The role of glutathione in the acute nephrotoxicity of sodium dichromate in ARCHIVES OF TOXICOLOGY
  • 1988-01. Renal function of chrome-plating workers and welders in INTERNATIONAL ARCHIVES OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH
  • 2001-06. In vivo reduction of chromium (VI) and its related free radical generation in MOLECULAR AND CELLULAR BIOCHEMISTRY
  • 1991-10. In vivo nephrotoxicity induced in mice by chromium(VI) in BIOLOGICAL TRACE ELEMENT RESEARCH
  • 1994-02. Role of cellular antioxidants in metal-induced damage in CELL BIOLOGY AND TOXICOLOGY
  • Journal

    TITLE

    BMC Nephrology

    ISSUE

    1

    VOLUME

    6

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/1471-2369-6-4

    DOI

    http://dx.doi.org/10.1186/1471-2369-6-4

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1019918557

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/15854231


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    343 schema:name Departamento de Nefrología, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano #1, Col Sección XVI, 14080 Tlalpan, México, D.F., México
    344 rdf:type schema:Organization
    345 grid-institutes:grid.9486.3 schema:alternateName Facultad de Medicina, Departamento de Farmacología, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria, 04510, México, D.F., México
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    347 Facultad de Química, Edificio B, Departamento de Química Analítica, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria 04510, México, D.F., México
    348 Facultad de Química, Edificio B, Laboratorio 124, Departamento de Química Orgánica, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria 04510, México, D.F., México
    349 schema:name Facultad de Medicina, Departamento de Farmacología, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria, 04510, México, D.F., México
    350 Facultad de Química, Departamento de Biología, Edificio B, Segundo Piso, Laboratorio 209, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria, 04510, México, D.F., México
    351 Facultad de Química, Edificio B, Departamento de Química Analítica, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria 04510, México, D.F., México
    352 Facultad de Química, Edificio B, Laboratorio 124, Departamento de Química Orgánica, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria 04510, México, D.F., México
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