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.