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Abstract Title:

Naringenin protects against cadmium-induced oxidative renal dysfunction in rats.

Abstract Source:

Toxicology. 2009 Feb 4;256(1-2):128-34. Epub 2008 Nov 21. PMID: 19063931

Abstract Author(s):

J Renugadevi, S Milton Prabu

Article Affiliation:

Department of Zoology, Annamalai University, Annamalainagar 608 002, Tamil Nadu, India.

Abstract:

Cadmium (Cd) is an environmental and industrial pollutant that affects various organs in human and experimental animals. Naringenin is a naturally occurring plant bioflavonoid found in citrus fruits, which has been reported to have a wide range of pharmacological properties. A body of evidence has accumulated implicating the free radical generation with subsequent oxidative stress in the biochemical and molecular mechanisms of cadmium toxicity. Since kidney is the critical target organ of chronic Cd toxicity, we carried out this study to investigate the effects of naringenin on Cd-induced toxicity in the kidney of rats. In experimental rats, oral administration of cadmium chloride (5mg/(kgday)) for 4 weeks significantly induced the renal damage which was evident from the increased levels of serum urea, uric acid, creatinine with a significant (p<0.05) decrease in creatinine clearance. Cadmium also significantly decreased the levels of urea, uric acid and creatinine in urine. A markedly increased levels of lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydroperoxides) and protein carbonyl contents with significant (p<0.05) decrease in non-enzymatic antioxidants (total sulfhydryl groups, reduced glutathione, vitamin C and vitamin E) and enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST)) as well as glutathione metabolizing enzymes (glutathione reductase (GR) and glutathione-6-phosphate dehydrogenase (G6PD)) were also observed in cadmium-treated rats. Co-administration of naringenin (25 and 50mg/(kgday)) along with Cd resulted in a reversal of Cd-induced biochemical changes in kidney accompanied by a significant decrease in lipid peroxidation and an increase in the level of renal antioxidant defense system. The histopathological studies in the kidney of rats also showed that naringenin (50mg/(kgday)) markedly reduced the toxicity of Cd and preserved the normal histological architecture of the renal tissue. The present study suggest that the nephroprotective potential of naringenin in Cd toxicity might be due to its antioxidant and metal chelating properties, which could be useful for achieving optimum effects in Cd-induced renal damage.

Study Type : Animal Study

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Sayer Ji
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