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Effect of Streptozotocin‐Induced Diabetes on Rat Brain Mitochondria
Author(s) -
Moreira P. I.,
Santos M. S.,
Moreno A. M.,
Proença T.,
Seiça R.,
Oliveira C. R.
Publication year - 2004
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2004.1107.x
Subject(s) - endocrinology , medicine , streptozotocin , cardiolipin , mitochondrion , oxidative stress , diabetes mellitus , malondialdehyde , glutathione , mitochondrial respiratory chain , biology , respiratory chain , citrate synthase , chemistry , enzyme , biochemistry , phospholipid , membrane
This study evaluated several parameters related to mitochondrial function and oxidative stress in streptozotocin (STZ)‐treated rats, a model of type 1 diabetes. For this purpose, the respiratory indexes (RCR and ADP/O ratio), mitochondrial transmembrane potential (ΔΨm), repolarization lag phase, repolarization level, mitochondrial enzymatic activities, ATP and malondialdehyde (MDA) levels, reduced glutathione (GSH), vitamin E and cardiolipin contents were determined in rat brain mitochondria isolated after 4 and 9 weeks after STZ treatment. Brain mitochondria isolated from citrate (vehicle)‐treated Wistar rats were used as control. We observed that STZ‐induced diabetes did not substantially affect brain mitochondrial function. Instead, 4‐week diabetic rats presented higher mitochondrial respiratory chain enzymatic activities, especially succinate‐cytochrome C reductase activity, compared to 4‐week control rats. In 9‐week diabetic rats, only a significant decrease in cardiolipin content was observed; however, a significant increase in mitochondrial GSH content occurred. All other parameters analysed remained statistically unchanged. From these results, we conclude that STZ‐induced diabetes did not promote brain mitochondrial dysfunction, suggesting that oxidative stress associated with type 1 diabetes is not directly related to mitochondrial dysfunction, but probably is related to extramitochondrial factor(s).