Nephroprotective Effect of Low Viscosity Sodium Alginate on Lead Acetate-Induced Nephrotoxicity in Rats

Abstract:

Objective: Renal failure in majority of population is considered to be idiopathic. Heavy metals like lead in drinking water are usually the hidden cause of these renal consequences. Thus, this study has been designed to investigate the effect of low viscosity sodium alginate (LvSA) in Lead-induced nephrotoxicity. Methods: Lead (0.2% lead acetate in drinking water for 5 weeks) was administered in rats to produce nephrotoxicity assessed in terms of histopathological changes, increase in serum creatinine, blood urea nitrogen, urinary N-acetyl-β D glucosaminidase (NAG), proteinuria, Thiobarbituric acid reactive substances (TBARS) and decrease in reduced glutathione level. Results: Lead acetate (LA) intoxication shown elevations in serum creatinine, Proteinuria, glomerular filtration rate (GFR), blood urea nitrogen (BUN), Thiobarbituric acid reactive substances (TBARS), altered urinary N-acetyl-β D glucosaminidase (NAG), kidney weight/ body weight ratio (KW/BW %), and creatinine clearance that indicate renal damage. Treatment with Low viscosity sodium alginate (LvSA) show significant decrease in serum creatinine, BUN, urinary NAG, protein in urine, KW/BW %, TBARS level and increase in GSH, creatinine clearance and GFR. Conclusion: Thus, on the basis of results it may be concluded that LvSA significantly attenuated Lead-induced nephrotoxicity.

Key words: Lead acetate nephrotoxicity, Glomerular blood flow, Oxidative stress, Low viscosity sodium alginate, Proximal convoluted tubules.