TY - JOUR
T1 - Effects of lecithinized superoxide dismutase on traumatic brain injury in rats
AU - Yunoki, Masatoshi
AU - Kawauchi, Masamitsu
AU - Ukita, Naoya
AU - Noguchi, Yasuhiro
AU - Nishio, Shinsaku
AU - Ono, Yasuhiro
AU - Asari, Shoji
AU - Ohmoto, Takashi
AU - Asanuma, Masato
AU - Ogawa, Norio
PY - 1997/10
Y1 - 1997/10
N2 - Only small amounts of superoxide dismutase (SOD) are present in the extracellular space to scavenge excess amounts of superoxide anions (O2-) released after traumatic brain injury (TBI). Experiments were performed in rats with cerebral contusion produced by weight-drop technique. 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 determined by tissue- specific gravity, administration of PC-SOD reduced brain edema in the periphery of the lesion 6 h after contusion. SOD activity increased in the peripheral region at 30 min after contusion, but returned to normal levels at 6 h after TBI. Administration of PC-SOD increased SOD activity up to 6 h after TBI. The expression of Cu, Zn-SOD mRNA increased in the core region, peripheral portion, and contralateral hemisphere up to 6 h after TBI, then was suppressed in all three 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 diminishes brain edema through a protective effect against O2-.
AB - Only small amounts of superoxide dismutase (SOD) are present in the extracellular space to scavenge excess amounts of superoxide anions (O2-) released after traumatic brain injury (TBI). Experiments were performed in rats with cerebral contusion produced by weight-drop technique. 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 determined by tissue- specific gravity, administration of PC-SOD reduced brain edema in the periphery of the lesion 6 h after contusion. SOD activity increased in the peripheral region at 30 min after contusion, but returned to normal levels at 6 h after TBI. Administration of PC-SOD increased SOD activity up to 6 h after TBI. The expression of Cu, Zn-SOD mRNA increased in the core region, peripheral portion, and contralateral hemisphere up to 6 h after TBI, then was suppressed in all three 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 diminishes brain edema through a protective effect against O2-.
KW - Brain edema
KW - Lecithinization
KW - Reactive oxygen species
KW - Superoxide dismutase
KW - Traumatic brain injury
KW - mRNA
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U2 - 10.1089/neu.1997.14.739
DO - 10.1089/neu.1997.14.739
M3 - Article
C2 - 9383092
AN - SCOPUS:0030724682
VL - 14
SP - 739
EP - 746
JO - Central Nervous System Trauma
JF - Central Nervous System Trauma
SN - 0897-7151
IS - 10
ER -