Neurological recovery from closed head injury is impaired in diabetic rats

Citation
V. Elangovan et al., Neurological recovery from closed head injury is impaired in diabetic rats, J NEUROTRAU, 17(11), 2000, pp. 1013-1027
Citations number
53
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROTRAUMA
ISSN journal
08977151 → ACNP
Volume
17
Issue
11
Year of publication
2000
Pages
1013 - 1027
Database
ISI
SICI code
0897-7151(200011)17:11<1013:NRFCHI>2.0.ZU;2-C
Abstract
Diabetes mellitus is a metabolic disorder associated with central nervous s ystem impairments. Recent studies implicate oxidative stress mediated by re active oxygen species (ROS) in the pathogenesis of diabetic complications. ROS have been shown to play role in the pathophysiology of brain injury. In the present study, closed head injury (CHI) was induced in diabetic rats t o test the hypothesis that chronic oxidative stress exacerbates brain damag e following CHI. Neurological recovery, edema, levels of low molecular weig ht antioxidants (LMWA), and markers of lipid peroxidation were determined a t different intervals after injury. Diabetic rats (4 weeks after induction with streptozotocin) were subjected to CHI. Brain edema (percent water) and clinical status (neurological severity score) were assessed during 7 days. Brain LMWA were determined using cyclic voltammetry (CV) and HPLC-EC. In a ddition, conjugated dienes and thiobarbituric acid reactive substances (TBA RS) were measured. Diabetic-CHI rats exhibited a lower rate of recovery and greater and more sustained edema (p < 0.01), as compared with the controls . At all times diabetic rats had higher levels of TEARS and conjugated dien es and lower concentrations of LMWA, and of vitamins C and E, suggesting ch ronic oxidative stress. At 5 min of CHI, the amounts of LMWA in control-CHI brains decreased (<similar to>50%,p < 0.01) and returned to normal by 48 h and 7 days. In the diabetic-CHI brain only one class of LMWA slightly decl ined but remained low for 7 days. The present results support the hypothesi s that diabetic rats are under chronic oxidative stress, and suffer greater neurological dysfunction, associated with further lipid peroxidation follo wing CHI.