Linked Life Data

9661912

Source:http://linkedlifedata.com/resource/pubmed/id/9661912

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1998-7-22
pubmed:abstractText
Prolonged hyperglycemia results in a number of diabetic complications, including retinopathy. Pericyte degeneration is one of the earliest histological changes observed in the development of diabetic retinopathy. Increased free radicals generated under hyperglycemia could damage the retina, which abounds in polyunsaturated fatty acids. In the current study, a severalfold increase in thiobarbituric acid-reactive substances was found in rat retina cultured in hyperglycemic medium, which decreased significantly when trolox, an amphipathic antioxidant, was included in the medium. To examine the contribution of oxidative stress in vivo, diabetic rats were fed trolox (0.4% in the diet) during the course of the experiments. After 5 mo of hyperglycemia, whole mounts of retinal vessels were prepared and endothelial cells (E) and pericytes (P) were counted. The ratio of E/P in the retinas obtained from normal rats, diabetic rats, and diabetic rats fed trolox were 1.74 +/- 0.186, 3.78 +/- 0.47, and 2.32 +/- 0.24, respectively. A significant restoration of pericytes by trolox suggests the involvement of oxidative injury during pericyte loss in diabetic retinopathy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1528-7394
pubmed:author
pubmed:issnType
Print
pubmed:day
24
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
467-75
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Prevention of pericyte loss by trolox in diabetic rat retina.
pubmed:affiliation
Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston 77555-0647, USA. ansari@utmb.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't