Title of article :
Modulatory effects of N-acetylcysteine on hyperoxaluric manifestations in rat kidney
Author/Authors :
Bijarnia، نويسنده , , Rakesh K. and Kaur، نويسنده , , Tanzeer and Aggarwal، نويسنده , , Kanika and Singla، نويسنده , , S.K. and Tandon، نويسنده , , Chanderdeep، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2008
Pages :
5
From page :
2274
To page :
2278
Abstract :
Hyperoxaluria is a condition where excessive oxalate is present in the urine. Many reports have documented free radical generation followed by hyperoxaluria as a consequence of which calcium oxalate deposition occurs in the kidney tissue. The present in vivo study was designed to investigate the potential of N-acetylcysteine in modulating hyperoxaluric manifestation induced by sodium oxalate in the rat kidneys. Male wistar rats in one group were administered single dose of sodium oxalate (70 mg/kg body weight) intraperitoneally to induce hyperoxaluric conditions and in the other group, rats were injected N-acetylcysteine (NAC) (200 mg/kg body weight) intraperitoneally, half an hour after sodium oxalate dose. The treatment is for a period of 24 h. N-acetylcysteine significantly reduced hyperoxaluria caused oxidative stress by reducing lipid peroxidation, restoring antioxidant enzymes activity in kidney tissue, followed by reduction in impairment of renal functioning. In addition, NAC administration reduced the number of calcium oxalate monohydrate (COM) crystals in the urine as observed under polarization microscope. Histological analysis depicted that NAC treatment decreased renal epithelial damage, inflammation and restored normal glomeruli morphology. Thus, it shows that use of an extraneous antioxidant may prove beneficial for combating the conditions of oxidative stress produced by hyperoxaluria.
Keywords :
Creatinine , Lipid peroxidation , oxidative stress , N-Acetylcysteine , urea , hyperoxaluria
Journal title :
Food and Chemical Toxicology
Serial Year :
2008
Journal title :
Food and Chemical Toxicology
Record number :
2120067
Link To Document :
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