Production of hydroxyl free radical by brain tissues in hyperglycemic ratssubjected to transient forebrain ischemia

Citation
Pa. Li et al., Production of hydroxyl free radical by brain tissues in hyperglycemic ratssubjected to transient forebrain ischemia, FREE RAD B, 27(9-10), 1999, pp. 1033-1040
Citations number
59
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL BIOLOGY AND MEDICINE
ISSN journal
0891-5849 → ACNP
Volume
27
Issue
9-10
Year of publication
1999
Pages
1033 - 1040
Database
ISI
SICI code
0891-5849(199911)27:9-10<1033:POHFRB>2.0.ZU;2-V
Abstract
Preischemic hyperglycemia is known to aggravate brain damage resulting from transient ischemia. In the study, we explored whether this aggravation is preceded by an enhanced formation of reactive oxygen species (ROS) during t he early reperfusion period. To that end, normo- and hyperglycemic rats wer e subjected to 15 min of forebrain ischemia and allowed recovery periods of 5, 15, and 60 min. Sodium salicylate was injected intraperitoneally in a d ose of 100 mg/kg, and tissues were sampled during recirculation to allow an alyses of salicylic acid (SA) and its hydroxylation products, 2,3- and 2,5- dihydroxybenzoate (DHBA). Tissue sampled from thalamus and caudoputamen in normoglycemic animals failed to show an increase in 2,3- or 2,5-DHBA after 5 and 15 min of recirculation. However, such an increase was observed in th e neocortex after 60 min of recirculation, with a suggested increase in the hippocampus as well. Hyperglycemia had three effects. First, it increased 2,5-DHBA in the thalamus and caudoputamen to values exceeding normoglycemic ones after 15 min of recirculation Second, it increased basal values of 2, 5- and total DHBA in the neocortex. Third, it increased the 60-min values f or 2,5- and total DHBA in the hippocampus. These results hint that, at leas t in part, hyperglycemia may aggravate damage by enhancing basal- and ische mia-triggered production of ROS. (C) 1999 Elsevier Science Inc.