Linked Life Data

19362073

Source:http://linkedlifedata.com/resource/pubmed/id/19362073

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2009-8-3
pubmed:abstractText
Neuronal malfunction is a characteristic feature of diabetic mellitus. Hence, the present study therefore sought to evaluate the effect of diphenyl diselenide (DPDS) on the antioxidant status, sodium pump, cholinergic and glutamatergic system in the rat brain of streptozotocin (STZ) induced diabetes. The results show that although STZ evoke a significant diminution on the antioxidant status and activity of Na(+)/K(+)-ATPase, the activity of acetylcholinesterase and glutamate uptake and release was not altered. However, DPDS was able to markedly restore the observed imbalance in cerebral antioxidant status and also relieve the inhibition of Na(+)/K(+)-ATPase caused by streptozotocin. Hence, we conclude that DPDS is a potential candidate in the management of neuronal dysfunction that often accompanied complications associated with diabetic hyperglycemia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1872-6240
pubmed:author
pubmed:issnType
Electronic
pubmed:day
11
pubmed:volume
1284
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
202-11
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Diphenyl diselenide and streptozotocin did not alter cerebral glutamatergic and cholinergic systems but modulate antioxidant status and sodium pump in diabetic rats.
pubmed:affiliation
Postgraduate Programme in Biochemical Toxicology, Centre for Natural and Exact Sciences, Federal University of Santa Maria, CEP 97105-900, Camobi, Santa Maria, RS, Brazil. ijkade@yahoo.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't