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Pharmacologia Vol. 5 (6), 2014
Research Article
Protective Effect of Naringin on Sodium Arsenite Induced Testicular Toxicity via Modulation of Biochemical Perturbations in Experimental Rats
MohammadAdil , AsjadVisnagri , V.Shiva Kumar , AmitD. Kandhare , Pinaki Ghosh and Subhash L. Bodhankar
 
Abstract: Background: Arsenicals induced testicular cancer is a serious debilitating epidemic affecting all social strata in developing as well as developed countries. Naringin possess antioxidant and free radical scavenging properties. Hence, the present investigation was design to elucidate the effect of naringin against sodium arsenite induced testicular toxicity in laboratory rats. Materials and Methods: Male Sprague-Dawley rats were pretreated with either vehicle (control), naringin (20, 40 and 80 mg kg-1, p.o.) and Co-enzyme Q10 (10 mg kg-1, p.o) for 7 days. Testicular toxicity was induced by sodium arsenite (10 mg kg-1, p. o., for two consecutive days). Drug treatment was continued up to 15th day. On 16th day reproductive organo-somatic indices, biochemical and histolopathogical determinations were carried out. Results: Rats pretreated with naringin (40 and 80 mg kg-1, p.o.) showed significant and dose dependant increased (p<0.01 and 0.001, respectively) in relative organ weight (epididymis, seminal vesicle and testis) and sperm count. It also showed significant increased (p<0.01 and 0.001, respectively) in level of serum protein, albumin, AST, ALT and activity of testicular endogenous enzymes (nitric oxide (NO) content superoxide dismutase (SOD) and reduced glutathione (GSH). The elevated levels of serum creatinine and glucose, testicular MDA and NO were significantly inhibited (p<0.01 and 0.001, respectively) by the naringin (40 and 80 mg kg-1, p.o.). It significantly (p<0.01) restored the alteration in serum lipid profile. Elevated levels of pro-inflammatory cytokines (Tumor necrosis factor-alpha (TNF-α) and Interleukin-1beta (IL-1β) were significantly and dose dependently (p<0.01 and 0.001, respectively) inhibited by the naringin (40 and 80 mg kg-1, p.o.) treatment. It also restored the histological aberration induced by the sodium arsenite. Conclusion: Naringin exerted its protective effects against sodium arsenite induced testicular toxicity via modulation of endogenous antioxidant enzyme, inhibition of release of oxido-inflammatory mediators such as MDA and NO as well as pro-inflammatory cytokines.
 
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