O. Yavuz et al., THE EFFECT OF 2-CHLOROADENOSINE ON LIPID PEROXIDE LEVEL DURING EXPERIMENTAL CEREBRAL ISCHEMIA-REPERFUSION IN GERBILS, Free radical biology & medicine, 22(1-2), 1997, pp. 337-341
Oxygen free radicals may be implicated in the pathogenesis of ischemia
-reperfusion damage. It is known that 2-chloroadenosine (2-CADO) has n
euromodulatory effects and prevents the neuronal damage seen in the pe
riod of postischemia reperfusion. However, direct effects of 2-CADO on
lipid peroxidation have not been investigated previously. The attack
on the cell membrane by free radicals leads to lipid peroxidation, whi
ch can be assayed by the malondialdehyde (MDA) level. The aim of this
study was to determine the effect of 2-CADO therapy on lipid peroxidat
ion in experimental forebrain ischemia and postischemia reperfusion in
Mongolian gerbils. Cerebral ischemia was induced by a bilateral 30-mm
occlusion of the common carotid arteries, 2-Chloroadenosine (0.6 mg/k
g, IV) was administered 5 min subsequent to ischemia. Ischemia was fol
lowed by reperfusion for 30 min. The MDA level was measured by the thi
obarbituric acid (TEA) test. Bilateral carotid artery occlusion for 30
min in gerbils resulted in no significant change in MDA level in the
brain. The MDA level was higher in postischemia reperfusion than in th
e ischemic group. 2-Chloroadenosine treatment did not change the MDA l
evel in the ischemic period. However, the MDA level recovered signific
antly upon 2-CADO therapy during reperfusion following ischemia. These
results suggest that 2-CADO may offer some degree of protection again
st oxidative stress in cerebral ischemia-reperfusion damage. Copyright
(C) 1996 Elsevier Science Inc.