Linked Life Data

16118484

Source:http://linkedlifedata.com/resource/pubmed/id/16118484

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-10-10
pubmed:abstractText
Oxidative stress has been considered to be a common pathogenetic factor of diabetic nephropathy. But the reason why renal cells are susceptible to oxidative injury in diabetes is not clear. Vitamin C plays a central role in the antioxidant defense system and exists in two major forms. The charged form, ascorbate, is taken up into cells via sodium-dependent facilitated transport. The uncharged form, dehydroascorbate, enters cells via glucose transporter and is then converted back to ascorbate within these cells. Because dehydroascorbate and glucose compete for glucose transporters, hyperglycemia will exclude vitamin C from the cell and resulted in a decreased antioxidant capacity in some cell type that is dehydroascorbate dependent. As such, we hypothesized that some renal cells were dehydroascorbate dependent and the susceptibility of renal cells to glucose-induced injury was mediated by hyperglycemic exclusion of dehydroascorbate uptake through competing for glucose transporter. The aims of the present study were to determine whether tubular epithelial cell was dehydroascorbate dependent and the effect of dehydroascorbate on the production of reactive oxygen species in cells incubated by high glucose.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0250-8095
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2005 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
459-65
pubmed:dateRevised
2007-2-14
pubmed:meshHeading
pubmed:articleTitle
Hyperglycemia inhibits the uptake of dehydroascorbate in tubular epithelial cell.
pubmed:affiliation
Division of Nephrology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan 430060, China.
pubmed:publicationType
Journal Article