Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02003 (NBT)
 1,323 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the potential role of SOD, an oxygen free radical scavenger, as a probe to cover the trigger period of injury and the prolonged period of development of edema in vasogenic brain edema. Vasogenic brain edema was produced in 34 cats by a standardized cortical freezing lesion. Brain edema and the disruption in the BBB were assessed by SG measurement and spread of Evans blue by planimetry. Detection of superoxide radicals was studied by topical application of NBT within the cranial window. Animals were separated into two groups: (a) controls; and (b) two SOD-treated groups--A was pretreated with 10,000 U/kg PEG-SOD intraperitoneally and sacrificed at 24 and 48 hr after lesions, and B received both a bolus injection of free SOD (4 mg/kg) and then 1 mg/kg/min for 20 min after the lesion and was sacrificed 6 hr later. Our preliminary data indicate that superoxide radicals were detected in the brain after cold-induced injury, but free and PEG-SOD had no beneficial effect on vasogenic brain edema produced by cold-induced injury. It is concluded that intracellular uptake of SOD might be necessary for an effect in the treatment of cold-induced brain edema.
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PMID:Effect of superoxide dismutase in cats with cold-induced edema. 216 63

We evaluated the effect of SOD, an oxygen-free radical scavenger, on peritumoral edema in 20 rabbits. The VX2 carcinoma was transplanted to the brains of these New Zealand white rabbits. Detection of superoxide radicals in vitro was performed by incubating the VX2 tumor cells with NBT. For evaluation of the effect of SOD on the tumor cells, they were treated with free SOD or PEG-SOD before and after incubation with NBT. The animals were separated into three groups: group 1, control group; group 2, SOD-untreated tumor group; group 3, two SOD-treated groups-group 3a, treated with 10,000 U/kg PEG-SOD on day 1 and 4 after tumor transplantation and sacrificed on day 13; group 3b, treated with 10,000 U/kg PEG-SOD on day 7 and 10 and sacrificed on day 13. Brain edema was assessed by SG measurement. Our preliminary in vitro data indicated that the VX2 carcinoma produced superoxide radicals but that free SOD and PEG-SOD could not penetrate into tumor cells nor inhibit superoxide radicals. In vivo data also indicated that PEG-SOD failed to reduce peritumoral edema. It was concluded that intracellular uptake or penetration of SOD must first be achieved before any effect on peritumoral edema can be assessed.
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PMID:Effect of superoxide dismutase in rabbits with peritumoral edema. 216 69

Only small amounts of superoxide dismutase (SOD) are present in the extracellular space to scavenge excess amounts of superoxide anions (02-) 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 02- 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 02- in the development of brain edema after TBI and indicate that PC-SOD diminishes brain edema through a protective effect against 02-.
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PMID:Effects of lecithinized superoxide dismutase on traumatic brain injury in rats. 938 92

To analyze the effect of lecithinized superoxide dismutase (SOD) on superoxide accumulation after traumatic brain injury (TBI) in rats, we studied the SOD activity by NBT-reducing method and the expression of Cu,Zn-SOD mRNA by Northern blot analysis. As determined by the specific gravity method, the administration of lecithinized SOD decreased brain edema in the periphery of the lesion at 6 hr after contusion. SOD activity, without lecithinized SOD administration, increased at the peripheral portion at 30 min after contusion, but decreased to normal level at 6 hr after TBI. By administration of lecithinized SOD, the increase of SOD activity was preserved until 6 hr after TBI. The expression of Cu,Zn-SOD mRNA increased in the core lesion, peripheral portion, and contralateral hemisphere until 6 hr after TBI, then was suppressed in all three areas by lecithinized SOD. These results support the hypothesis that superoxide anions may play an important role in the development of brain edema after TBI, and that leciyhinized SOD appears to prevent brain edema through a protective effect against superoxide anions.
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PMID:Effects of lecithinized SOD on sequential change in SOD activity after cerebral contusion in rats. 977 68