Protective effect of naringin, a bioflavonoid on ferric nitrilotriacetate-induced oxidative renal damage in rat kidney

An iron chelate, ferric nitrilotriacetate (Fe–NTA), induces acute proximal tubular necrosis as a consequence of lipid peroxidation and oxidative tissue damage that eventually leads to high incidence of renal adenocarcinomas in rodents. This study was designed to investigate the effect of Naringin, a...

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Bibliographic Details
Published in:Toxicology (Amsterdam) 2004-09, Vol.201 (1), p.1-8
Main Authors: Singh, Devinder, Chander, Vikas, Chopra, Kanwaljit
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Chelating Agents - toxicity
Creatinine - blood
Dose-Response Relationship, Drug
Flavanones - therapeutic use
Kidney Diseases - chemically induced
Kidney Diseases - pathology
Kidney Diseases - prevention & control
Lipid Peroxidation - drug effects
Male
Medical sciences
Naringin
Nitrilotriacetic acid
Nitrilotriacetic Acid - antagonists & inhibitors
Nitrilotriacetic Acid - toxicity
Oxidative stress
Rats
Rats, Wistar
Superoxide Dismutase - metabolism
Toxicology
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Summary:An iron chelate, ferric nitrilotriacetate (Fe–NTA), induces acute proximal tubular necrosis as a consequence of lipid peroxidation and oxidative tissue damage that eventually leads to high incidence of renal adenocarcinomas in rodents. This study was designed to investigate the effect of Naringin, a bioflavonoid with anti-oxidant potential, on Fe–NTA-induced nephrotoxicity in rats. One hour after a single intra-peritoneal (i.p.) injection of Fe–NTA (8 mg iron/kg body weight), a marked deterioration of renal architecture and renal function was observed. Fe–NTA induced a significant renal oxidative stress, demonstrated by elevated thiobarbituric acid reacting substances (TBARS) and reduction in activities of renal catalase, superoxide dismutase, and glutathione reductase. Pre-treatment of animals with Naringin, 60 min before Fe–NTA administration, markedly attenuated renal dysfunction, morphological alterations, reduced elevated TBARS, and restored the depleted renal anti-oxidant enzymes. These results clearly demonstrate the role of oxidative stress and its relation to renal dysfunction and suggest a protective effect of Naringin on Fe–NTA-induced nephrotoxicity in rats.
ISSN:0300-483X
1879-3185
DOI:10.1016/j.tox.2004.03.028