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Deleterious effects of oxidative and nitrosative stress on aconitase activity in brain mitochondria during diabetes
Author(s) -
NoriegaCisneros Ruth,
EsquivelGutiérrez Edgar,
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
Subject(s) - aconitase , diabetes mellitus , oxidative stress , endocrinology , medicine , streptozotocin , mitochondrion , peroxynitrite , nitric oxide , chemistry , superoxide , biochemistry , enzyme
In diabetes mellitus it is found diabetic encephalopathy. Chronic hyperglycemia induces an increment in glycemia oxidation when is oxidized the mitochondrial respiratory chain generate superoxide and oxidative stress. Aconitase possess a particular characteristic susceptible to oxidative damage. In this study it was analyzed the roles of mtNO, superoxide radical and peroxynitrite generation under diabetes on aconitase activity. We used streptozotocin‐induced diabetes rats of different ages and brain mitochondria were isolated. Brain mitochondria NO levels were 13 and 14 nmoles/mg/ml in control and diabetic rats, respectively, of 1 week diabetes treatment. These values diminished to 69% in the control rats, compared to a decrease of 57% in the diabetic rats of 7 weeks diabetic treatment. Aconitase activity values in brain mitochondria of 1 week diabetes treatment diminished from 100% to 85%. In diabetic rats with seven week streptozotocin‐induced diabetes, aconitase activity decreased from 45% in the control to 20% in the diabetic rats. The results are in accordance with our hypothesis that aging in diabetic rats affect both mitochondrial nitric oxide and aconitase activity. Acknowledgements: The authors appreciate the partial economic support from the grants of CONACYT (43705) and CIC‐UMSNH (2.16‐2006).

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