Effect of NADPH oxidase inhibition on the expression of kidney injury molecule and calcium oxalate crystal deposition in hydroxy-L-proline-induced hyperoxaluria in the male Sprague-Dawley rats
Author(s) -
Jianping Zuo,
Aslam Khan,
Patricia A. Glenton,
Saeed R. Khan
Publication year - 2011
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfr035
Subject(s) - apocynin , endocrinology , medicine , kidney , nadph oxidase , calcium oxalate , excretion , osteopontin , nicotinamide adenine dinucleotide phosphate , oxalate , urinary system , oxidase test , chemistry , biochemistry , oxidative stress , enzyme , organic chemistry
Renal calcium oxalate (CaOx) crystal deposition is associated with epithelial injury and movement of inflammatory cells into the interstitium. We have proposed that oxalate (Ox)- and CaOx crystal-induced injury is most likely caused by reactive oxygen species (ROS) produced by activation of membrane nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.
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