Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04179 (MnSOD)
 2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have characterized the temporal changes in iNOS, MnSOD and nitrotyrosine immune reactivity in a rat model of permanent middle cerebral artery occlusion under acute hyperglycemic or normoglycemic conditions followed by either 3- or 24-h recovery. We found that the macroscopic labeling pattern for all three antibodies colocalized with the ischemic core and penumbra which was determined by cresyl violet histological evaluation in adjacent sections. Hyperglycemia induced prior to ischemia resulted in earlier infarction which correlated with increased immunoreactivity for iNOS, MnSOD and nitrotyrosine. In the penumbral region of the frontal cortex, labeling of specific cell structures was largely limited to cortical neurons near the corpus callosum and was apparent earlier in the hyperglycemic rats. Increased polymorphonuclear leukocyte adhesion in blood vessels was observed at 24 h in the hyperglycemic group. At both of the recovery times studied, we observed only minor vascular staining for nitrotyrosine and none for iNOS. Our results are consistent with hyperglycemia resulting in an early and concomitant increase in both superoxide and nitric oxide production which can lead to peroxynitrite formation that then nitrates tyrosine residues. It would appear that hyperglycemic ischemia contributes to the early induction of key enzymes involved in nitric oxide bioavailability.
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PMID:Immunohistochemical detection of inducible nitric oxide synthase, nitrotyrosine and manganese superoxide dismutase following hyperglycemic focal cerebral ischemia. 1168 37

The period from stroke initiation to the cessation of penumbra damage spread represents a therapeutic window when expansion can be alleviated. In the present work, we studied some biochemical parameters helpful for the estimation of infarct progression and thus for the application of interventions. We designed four groups: the control group and three groups of animals after middle cerebral artery occlusion with reperfusion periods of 2h, 1day or 3days. In the ischaemic core and penumbra, fluorimetric and spectrophotometric methods for investigating total MnSOD and MAO-A/B activity as well as level of the glutamate were used. Protein synthesis was assessed by in vitro measurements of (14)C-leucine incorporation. Noticeable differences between core and penumbra biochemical parameters were shown. In the core, protein synthesis was transiently inhibited two hours and three days after ischaemia (36%). Glutamate and total SOD activity peaked on the first day, but on the third day after MCAO, rapidly decreased by about 44% and 33.6%, respectively. In the penumbra, ischaemia led to higher protein synthesis (78%), elevations in glutamate and rapid activation of MnSOD (by about 884%) one day after insult. On the third day, protein synthesis and MnSOD were still significantly elevated (36% and 388%, respectively), while glutamate levels returned to baseline. In addition, the impact of ischaemia on MAO-A/B activity in the penumbra was confirmed. In conclusion, biochemical parameter screening could be helpful to assess cell damage progress and the possibility of rescue. These regions reflect different biochemical patterns that seem to be clearly established on the first day after transient MCAO. Moreover, the first day of post-ischaemic reperfusion in the present model of stroke seems to be the breakpoint, i.e. the time at which expanding cell death from the infarct core to the penumbra can be at least partially eliminated.
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PMID:Development of a pattern in biochemical parameters in the core and penumbra during infarct evolution after transient MCAO in rats. 2314 52