  Some markers of oxidative injury were measured in different rat brain areas
(hippocampus, cerebral cortex, striatum, hypothalamus, amygdala/piriform cortex
and cerebellum) after the systemic administration of an excitotoxic dose 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 glutathione (GSH)
levels in hippocampus, cerebellum and amygdala/piriform cortex (maximal
reduction at 24 h). In a similar way, lipid peroxidation, as assessed 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 after KA
application. On the other hand, brain areas such as hypothalamus, striatum and
cerebral cortex seem to be less susceptible to KA excitotoxicity. According to
these findings, the pattern of oxidative injury induced by systemically
administered KA seems to be highly region-specific. Further, our results have
shown that a lower antioxidant status (GSH and SOD) seems not to play an
important role in the selective vulnerability of certain brain regions because
it correlates poorly with increases in markers of oxidative damage.
