Free radicals are involved in the damage to protein synthesis after XXXX /aglycemia and NMDA exposure.

@entity1024 @entity270 @entity63 @entity1249 @entity3624 @entity16 @entity620 @entity898 @entity4053 @entity519 @entity460 @entity35
Neuronal protein synthesis is inhibited in @entity1249 pyramidal neurons for many hours after @entity63 , @entity519 or @entity4053 . This inhibition precedes cell death, is a hallmark characteristic of @entity16 and may play a key role in the death of vulnerable neurons after these insults. The sequence of events leading to this inhibition remains to be fully elucidated. The protein synthesis failure after 7.5 min @entity519 /aglycemia in the @entity35 hippocampal slice can be prevented by blocking @entity1024 receptors in a reduced @entity460 environment during the insult. In this study, we demonstrate that @entity1024 exposure directly causes a dose-dependent, receptor-mediated and prolonged protein synthesis inhibition in @entity1249 pyramidal neurons. The free radical scavenger @entity270 significantly attenuates this damage due to low concentrations of @entity1024 (10 microM). Free radical generation by @entity3624 / @entity3624 oxidase (XOD) can directly damage protein synthesis in neurons of the slice. @entity270 , @entity620 and @entity898 can each prevent the damage due to @entity519 /aglycemia and to higher concentrations of @entity1024 (50 microM), provided @entity460 levels are reduced concomitantly. These findings indicate that both free radicals and @entity460 play a role in the sequence of events leading to protein synthesis failure after energetic stress like @entity519 /aglycemia. They further suggest that the mechanism by which @entity1024 receptor activation damages protein synthesis involves free radical generation.
