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ROLE OF MITOCHONDRIAL NITRIC OXIDE AND REACTIVE OXYGEN SPECIES IN RAT KIDNEY DURING DIABETES
Author(s) -
EsquivelGutiérrez Edgar,
NoriegaCisneros Ruth,
ClementeGuerrero Mónica,
CaudilloNoriega Evangelina,
GutiérrezPérez Areli,
CalderónCortés Elizabeth,
CortésRojo Christian,
ManzoÁvalos Salvador,
SaavedraMolina Alfredo
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a668-a
Subject(s) - endocrinology , medicine , diabetes mellitus , diabetic nephropathy , nitric oxide , oxidative stress , peroxynitrite , kidney , nephropathy , insulin , streptozotocin , superoxide , chemistry , biochemistry , enzyme
Diabetes mellitus (DM) is a heterogeneous metabolic disorder characterized by hyperglycemia resulting from defective insulin secretion, resistance to insulin action or both. Oxidative damage due to hyperglycemia contributes to the microvascular pathology of diabetes that occurs in the renal glomerulus. The long‐term complications in DM include diabetic nephropathy. Veelken et al. (2000) tested that renal vasodilatation mediated by nitric oxide (NO) is due to endothelial constitutive nitric oxide synthase (eNOS) activity and contributed to hyperfiltration and renal injury in diabetic rats. NO is an important factor in the etiology and pathogenesis in early diabetic nephropathy of rats. Thereafter, our laboratory is interesting in the role of mitochondrial NO (mtNO) during diabetes in kidney of streptozotocin (STZ)‐induced diabetic rats. Our results showed that increased mtNO production is markedly high at the seven days after a single injection of STZ. We observed also at the end of seven and sixteen weeks less mtNO production, perhaps the mtNO is combined with superoxide anion to produce peroxynitrite, because the biological effects of NO are significantly mediated through S‐nitrosylation. In DM, oxidative stress seems mainly to be due to an increased production of free radical and/or a sharp reduction of antioxidant defense. Therefore, oxidative and nitrosative stress plays a central role in diabetic renal tissue damage. Acknowledgements: The authors appreciate the partial economic support from the grants of CONACYT (43705) and CIC‐UMSNH (2.16‐2006).