Only small amounts of superoxide dismutase (SOD) are present in the ex
tracellular space to scavenge excess amounts of superoxide anions (O2(
-)) released after traumatic brain injury (TBI). Experiments were perf
ormed in rats with cerebral contusion produced by weight-drop techniqu
e. We investigated the effects of exogenous lecithinized SOD (PC-SOD)
on accumulation of O2(-) produced in our model, by measuring the level
of SOD activity (using the NBT-reducing method) and the expression of
copper, zinc-SOD (Cu, Zn-SOD) mRNA (by Northern blot analysis). As de
termined by tissue-specific gravity, administration of PC-SOD reduced
brain edema in the periphery of the lesion 6 h after contusion. SOD ac
tivity increased in the peripheral region at 30 min after contusion, b
ut returned to normal levels at 6 h after TBI. Administration of PC-SO
D increased SOD activity up to 6 h after TBI. The expression of Cu, Zn
-SOD mRNA increased in the core region, peripheral portion, and contra
lateral hemisphere up to 6 h after TBI, then was suppressed in all thr
ee regions by PC-SOD. Our results confirm the important role of O2(-)
in the development of brain edema after TBI and indicate that PC-SOD d
iminishes brain edema through a protective effect against O2(-).