Abstract:
:Mitochondrial dysfunction and oxidative stress are implicated in the pathological changes observed in the diabetic central nervous system. In this study, using the streptozotocin-induced diabetic rat model we document for the first time the over-expression of a mitochondrial specific stress protein (chaperonin 60) in the CA1/CA3 regions of the diabetic hippocampus in the absence of neurodegeneration. The increase in expression of chaperonin 60 was not observed in the cohort treated with insulin, suggesting that the observed effect was not due to streptozotocin per se but due to the hyperglycaemic state induced by the diabetic state. The expression of chaperonin 60 was also positively correlated with a marker of mitochondrial oxidative stress (manganese superoxide dismutase). We suggest that chaperonin 60 could be an early event marker of mitochondrial dysfunction in the diabetic central nervous system and indeed be neuroprotective in the early stages of hyperglycaemic-induced oxidative stress.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Yuan J,Young BJ,Martinus RDdoi
10.1097/01.wnr.0000201503.15632.06subject
Has Abstractpub_date
2006-02-27 00:00:00pages
239-42issue
3eissn
0959-4965issn
1473-558Xpii
00001756-200602270-00003journal_volume
17pub_type
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