Hypothyroidism attenuates protein tyrosine nitration, oxidative stress and renal damage induced by ischemia and reperfusion: effect unrelated to antioxidant enzymes ... View Full Text


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Article Info

DATE

2005-11-07

AUTHORS

Verónica M Tenorio-Velázquez, Diana Barrera, Martha Franco, Edilia Tapia, Rogelio Hernández-Pando, Omar Noel Medina-Campos, José Pedraza-Chaverri

ABSTRACT

BACKGROUND: It has been established that hypothyroidism protects rats against renal ischemia and reperfusion (IR) oxidative damage. However, it is not clear if hypothyroidism is able to prevent protein tyrosine nitration, an index of nitrosative stress, induced by IR or if antioxidant enzymes have involved in this protective effect. In this work it was explored if hypothyroidism is able to prevent the increase in nitrosative and oxidative stress induced by IR. In addition the activity of the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase was studied. Control and thyroidectomized (HTX) rats were studied 24 h of reperfusion after 60 min ischemia. METHODS: Male Wistar rats weighing 380 +/- 22 g were subjected to surgical thyroidectomy. Rats were studied 15 days after surgery. Euthyroid sham-operated rats were used as controls (CT). Both groups of rats underwent a right kidney nephrectomy and suffered a 60 min left renal ischemia with 24 h of reperfusion. Rats were divided in four groups: CT, HTX, IR and HTX+IR. Rats were sacrificed and samples of plasma and kidney were obtained. Blood urea nitrogen (BUN) and creatinine were measured in blood plasma. Kidney damage was evaluated by histological analysis. Oxidative stress was measured by immunohistochemical localization of protein carbonyls and 4-hydroxy-2-nonenal modified proteins. The protein carbonyl content was measured using antibodies against dinitrophenol (DNP)-modified proteins. Nitrosative stress was measured by immunohistochemical analysis of 3-nitrotyrosine modified proteins. The activity of the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase was measured by spectrophotometric methods. Multiple comparisons were performed with ANOVA followed by Bonferroni t test. RESULTS: The histological damage and the rise in plasma creatinine and BUN induced by IR were significantly lower in HTX+IR group. The increase in protein carbonyls and in 3-nitrotyrosine and 4-hydroxy-2-nonenal modified proteins was prevented in HTX+IR group. IR-induced decrease in renal antioxidant enzymes was essentially not prevented by HTX in HTX+IR group. CONCLUSION: Hypothyroidism was able to prevent not only oxidative but also nitrosative stress induced by IR. In addition, the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase seem not to play a protective role in this experimental model. More... »

PAGES

12-12

References to SciGraph publications

  • 2000-02. Kidney ischemia-reperfusion: Modulation of antioxidant defenses in MOLECULAR AND CELLULAR BIOCHEMISTRY
  • 2004-09. Thyroid Hormone Influences Antioxidant Defense System in Adult Rat Brain in NEUROCHEMICAL RESEARCH
  • 2005-04-26. Time course study of oxidative and nitrosative stress and antioxidant enzymes in K2Cr2O7-induced nephrotoxicity in BMC NEPHROLOGY
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  • 2001-05-01. Influence of hyper‐ and hypothyroidism on lipid peroxidation, unsaturation of phospholipids, glutathione system and oxidative damage to nuclear and mitochondrial DNA in mice skeletal muscle in MOLECULAR AND CELLULAR BIOCHEMISTRY
  • 2005-09. Short-Term Thyroxine Administration Leads to Lipid Peroxidation in Renal and Testicular Tissues of Rats with Hypothyroidism in BIOLOGIA FUTURA
  • 2005-06. Changes in Antioxidant Status, Protein Concentration, Acetylcholinesterase, (Na+,K+)-, and Mg2+-ATPase Activities in the Brain of Hyper- and Hypothyroid Adult Rats in METABOLIC BRAIN DISEASE
  • 2003-10-31. The effect of dehydroepiandrosterone on renal ischemia-reperfusion-induced oxidative stress in rabbits in UROLITHIASIS
  • 2004-04-30. S-allylmercaptocysteine scavenges hydroxyl radical and singlet oxygen in vitro and attenuates gentamicin-induced oxidative and nitrosative stress and renal damage in vivo in BMC CLINICAL PHARMACOLOGY
  • 1999-06. Hypothyroidism Protects Rat Liver from Acetaminophen Hepatotoxicity in DIGESTIVE DISEASES AND SCIENCES
  • 2001-01. Post-transcriptional control of catalase expression in garlic-treated rats in MOLECULAR AND CELLULAR BIOCHEMISTRY
  • 1996-12. Sodium-dependent adenosine transport is diminished in brush border membrane vesicles from hypothyroid rat kidney in PFLÜGERS ARCHIV - EUROPEAN JOURNAL OF PHYSIOLOGY
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/1471-2369-6-12

    DOI

    http://dx.doi.org/10.1186/1471-2369-6-12

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1034475570

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/16274486


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    32 schema:description BACKGROUND: It has been established that hypothyroidism protects rats against renal ischemia and reperfusion (IR) oxidative damage. However, it is not clear if hypothyroidism is able to prevent protein tyrosine nitration, an index of nitrosative stress, induced by IR or if antioxidant enzymes have involved in this protective effect. In this work it was explored if hypothyroidism is able to prevent the increase in nitrosative and oxidative stress induced by IR. In addition the activity of the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase was studied. Control and thyroidectomized (HTX) rats were studied 24 h of reperfusion after 60 min ischemia. METHODS: Male Wistar rats weighing 380 +/- 22 g were subjected to surgical thyroidectomy. Rats were studied 15 days after surgery. Euthyroid sham-operated rats were used as controls (CT). Both groups of rats underwent a right kidney nephrectomy and suffered a 60 min left renal ischemia with 24 h of reperfusion. Rats were divided in four groups: CT, HTX, IR and HTX+IR. Rats were sacrificed and samples of plasma and kidney were obtained. Blood urea nitrogen (BUN) and creatinine were measured in blood plasma. Kidney damage was evaluated by histological analysis. Oxidative stress was measured by immunohistochemical localization of protein carbonyls and 4-hydroxy-2-nonenal modified proteins. The protein carbonyl content was measured using antibodies against dinitrophenol (DNP)-modified proteins. Nitrosative stress was measured by immunohistochemical analysis of 3-nitrotyrosine modified proteins. The activity of the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase was measured by spectrophotometric methods. Multiple comparisons were performed with ANOVA followed by Bonferroni t test. RESULTS: The histological damage and the rise in plasma creatinine and BUN induced by IR were significantly lower in HTX+IR group. The increase in protein carbonyls and in 3-nitrotyrosine and 4-hydroxy-2-nonenal modified proteins was prevented in HTX+IR group. IR-induced decrease in renal antioxidant enzymes was essentially not prevented by HTX in HTX+IR group. CONCLUSION: Hypothyroidism was able to prevent not only oxidative but also nitrosative stress induced by IR. In addition, the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase seem not to play a protective role in this experimental model.
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