Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/78324
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Type: Journal article
Title: Selenium inhibits renal oxidation and inflammation but not acute kidney injury in an animal model of rhabdomyolysis
Author: Shanu, A.
Groebler, L.
Kim, H.
Wood, S.
Weekley, C.
Aitken, J.
Harris, H.
Witting, P.
Citation: Antioxidants & Redox Signaling, 2013; 18(7):756-769
Publisher: Mary Ann Liebert, Inc. Publishers
Issue Date: 2013
ISSN: 1523-0864
1557-7716
Statement of
Responsibility: 
Anu Shanu, Ludwig Groebler, Hyun Bo Kim, Sarah Wood, Claire M. Weekley, Jade B. Aitken, Hugh H. Harris, and Paul K. Witting
Abstract: Acute kidney injury (AKI) is a manifestation of rhabdomyolysis (RM). Extracellular myoglobin accumulating in the kidney after RM promotes oxidative damage, which is implicated in AKI. AIM: To test whether selenium (Se) supplementation diminishes AKI and improves renal function. RESULTS: Dietary selenite increased Se in the renal cortex, as demonstrated by X-ray fluorescence microscopy. Experimental RM-stimulated AKI as judged by increased urinary protein/creatinine, clusterin, and kidney injury molecule-1 (KIM-1), decreased creatinine clearance (CCr), increased plasma urea, and damage to renal tubules. Concentrations of cholesterylester (hydro)peroxides and F₂-isoprostanes increased in plasma and renal tissues after RM, while aortic and renal cyclic guanidine monophosphate (cGMP; marker of nitric oxide (NO) bioavailability) decreased. Renal superoxide dismutase-1, phospho-P65, TNFα gene, MCP-1 protein, and the 3-chloro-tyrosine/tyrosine ratio (Cl-Tyr/Tyr; marker of neutrophil activation) all increased after RM. Dietary Se significantly decreased renal lipid oxidation, phospho-P65, TNFα gene expression, MCP-1 and Cl-Tyr/Tyr, improved NO bioavailability in aorta but not in the renal microvasculature, and inhibited proteinuria. However, CCr, plasma urea and creatinine, urinary clusterin, and histopathological assessment of AKI remained unchanged. Except for the Se++ group, renal angiotensin-receptor-1/2 gene/protein expression increased after RM with parallel increases in MEK1/2 inhibitor-sensitive MAPkinase (ERK) activity. INNOVATION: We employed synchrotron radiation to identify Se distribution in kidneys, in addition to assessing reno-protection after RM. CONCLUSION: Se treatment has some potential as a therapeutic for AKI as it inhibits oxidative damage and inflammation and decreases proteinuria, albeit histopathological changes to the kidney and some plasma and urinary markers of AKI remain unaffected after RM.
Keywords: Kidney; Animals; Rats; Rats, Sprague-Dawley; Rhabdomyolysis; Disease Models, Animal; Inflammation; Selenium; Tissue Distribution; Dietary Supplements; Male; Acute Kidney Injury
Rights: © Mary Ann Liebert, Inc.
RMID: 0020124691
DOI: 10.1089/ars.2012.4591
Grant ID: http://purl.org/au-research/grants/arc/DP0878559
http://purl.org/au-research/grants/arc/DP0985807
http://purl.org/au-research/grants/arc/LE100100125
Appears in Collections:IPAS publications
Environment Institute publications

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