Oxygen free radicals may be implicated in the pathogenesis of
ischemia-
reperfusion damage. It is known that
2-chloroadenosine (2-CADO) has neuromodulatory effects and prevents the neuronal damage seen in the period 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, which can be assayed by the
malondialdehyde (MDA) level. The aim of this study was to determine the effect of 2-CADO
therapy on lipid peroxidation 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/kg, IV) was administered 5 min subsequent to
ischemia.
Ischemia was followed by reperfusion for 30 min. The MDA level was measured by the
thiobarbituric acid (TBA) 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 the ischemic group.
2-Chloroadenosine treatment did not change the MDA level in the ischemic period. However, the MDA level recovered significantly upon 2-CADO
therapy during reperfusion following
ischemia. These results suggest that 2-CADO may offer some degree of protection against oxidative stress in
cerebral ischemia-
reperfusion damage.