Transient, global cerebral ischemia (TGCI) causes hippocampal/cortical damage and the persistent loss of welltrained,
long-term memory (retrograde amnesia). Fish oil (FO), a rich source of omega-3 polyunsaturated fatty acids,
abolishes such amnesia in the absence of neurohistological protection. The present study investigated whether FO
prevents ischemia-induced oxidative stress and whether such an action contributes to the lasting effect of FO on memory
recovery. In a first experiment, FO was administered for 4 days prior to ischemia, and antioxidant status was subsequently
measured after 24 h of reperfusion. In another experiment, naive rats were trained in an eight-arm radial maze until they
achieved asymptotic performance and then subjected to TGCI. One group of rats received FO as in the first experiment
(i.e., 4 days prior to ischemia), whereas another group received FO for 4 days prior to ischemia plus 6 days postischemia.
Retrograde memory performance was assessed 2-5 weeks after ischemia. TGCI depleted the level of antioxidant enzymes
and increased the amount of protein carbonylation, indicating oxidative damage. Fish oil reversed oxidative damage to
control levels. The same treatment that attenuated oxidative stress after 24 h of reperfusion also prevented retrograde
amnesia assessed several weeks later. This antiamnesic effect afforded by short preischemia treatment was comparable to
10 days of treatment but not as consistent. These data indicate that an antioxidant action in the hyperacute phase of
ischemia/reperfusion may contribute to the long-term, antiamnesic effect of FO.
Keywords: Fish oil, global cerebral ischemia, memory deficit, neurodegeneration, oxidative stress, recovery of function.
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