Renal injury mediated calcium oxalate nephrolithiasis: role of lipid peroxidation.
The role of lipid peroxidation (LPO) in renal tubular damage mediated calcium oxalate retention was investigated in a rat model. Hyperoxaluria, without deposition of oxalate in kidney, was induced by administration of ethylene glycol (EG), a precursor of oxalate. Oxidative stress condition was produced by administration of buthionine sulfoximine (BSO), an inhibitor of glutathione biosynthesis. BSO-treated rats showed a significant (p < 0.001) increase in LPO over EG-treated rats and it was almost doubled in BSO + EG treated rats. LPO was accompanied by significant urinary excretion of renal damage marker enzymes such as gamma-glutamyl transpeptidase (gamma-GT), alkaline phosphatase (ALP) and cathepsin D, mucoproteins, and glycosaminoglycans (GAGs) in the BSO and BSO + EG groups but not in the EG group. Urinary excretion of gamma-GT (r = +0.90) (p < 0.001) and deposition of oxalate (r = +0.78) (p < 0.001) in kidney positively correlated with LPO. These results suggest that LPO initiates renal damage, thereby leading to calcium oxalate retention and stone formation.
Muthukumar
A
A
Department of Medical Biochemistry Dr. A. L. M. Post-Graduate Institute of Basic Medical Sciences University of Madras Taramani, India.
Selvam
R
R
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D019328:Buthionine Sulfoximine / Q000633:toxicity; D002129:Calcium Oxalate / Q000378:metabolism*; D019855:Ethylene Glycol; D005026:Ethylene Glycols / Q000633:toxicity; D007668:Kidney / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D007669:Kidney Calculi / Q000139:chemically induced / Q000378:metabolism*; D015227:Lipid Peroxidation; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D005723:gamma-Glutamyltransferase / Q000378:metabolism
D005026:Ethylene Glycols; D002129:Calcium Oxalate; D019328:Buthionine Sulfoximine; D005723:gamma-Glutamyltransferase; D019855:Ethylene Glycol