Selective vulnerability to kainate-induced oxidative damage in different rat brain regions

Some markers of oxidative injury were measured in different rat brain areas (hippocampus, cerebral cortex, striatum, hypothalamus, amygdala/piriform c ortex and cerebellum) after the systemic administration of an excitotoxic d ose of kainic acid (KA, 9 mg kg(-1) i.p.) at two different sampling times ( 24 and 48 h). Kainic acid was able to lower markedly (P < 0.05) the glutath ione (GSH) levels in hippocampus, cerebellum and amygdala/piriform cortex ( maximal reduction at 24 h). In a similar way, lipid peroxidation, as assess ed by malonaldehyde and 4-hydroxyalkenal levels, significantly increased (P < 0.05) in hippocampus, cerebellum and amygdala/piriform cortex mainly at 24 h after KA. In addition, hippocampal superoxide dismutase (SOD) activity decreased significantly (P < 0.05) with respect to basal levels by 24 h af ter KA application. On the other hand, brain areas such as hypothalamus, st riatum and cerebral cortex seem to be less susceptible to KA excitotoxicity . According to these findings, the pattern of oxidative injury induced by s ystemically administered KA seems to be highly region-specific. Further, ou r results have shown that a lower antioxidant status (GSH and SOD) seems no t to play an important role in the selective vulnerability of certain brain regions because it correlates poorly with increases in markers of oxidativ e damage. Copyright (C) 2001 John Wiley & Sons, Ltd.