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HNE‐dependent molecular damage in diabetic nephropathy and its possible prevention by N‐acetyl‐cysteine and oxerutin
Author(s) -
Furfaro Anna Lisa,
Menini Stefano,
Patriarca Stefania,
Pesce Carlo,
Odetti Patrizio,
Cottalasso Damiano,
Marinari Umberto M.,
Adelaide Pronzato M.,
Traverso Nicola
Publication year - 2005
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520240134
Subject(s) - taurine , diabetic nephropathy , glycation , nephropathy , chemistry , diabetes mellitus , antioxidant , kidney , medicine , endocrinology , oxidative damage , oxidative stress , pharmacology , biochemistry , amino acid
Abstract Accumulation of Advanced Lipoxidation End‐products (ALE), such as MDA‐ and HNE‐protein adducts, and Advanced Glycation End‐products, such as carboxymethyl‐lysine (CML), are probably involved in the development of diabetic nephropathy. In this study the effect of some antioxidant treatments (oxerutin, N‐acetylcysteine, taurine and N‐acetylcysteine+taurine) on kidney lipoxidative damage has been evaluated by immunohistochemistry in streptozotocined rats. Diabetic rats showed marked glomerular positivity for ALE, while the samples from Control rats were negative. All treatments except taurine were able to protect the glomeruli from ALE accumulation; the failure of taurine may be due to residual oxidative properties of its derivatives. These data are consistent with those of our previous study, which showed that all the antioxidants used except taurine protected the glomeruli from diabetes‐induced enlargement, increased apoptotic rate, decreased cell density and CML accumulation. These data attest to a role of glycoxidative and lipoxidative damage in diabetes‐dependent damage of the kidney, and indicate that specific antioxidants can prevent or attenuate diabetic nephropathy.