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Are free radicals toxic to neurons? 

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These results suggest that free radicals derived from oxygen may attack nerve terminals and peroxidize the plasma membrane.
The ability of brain homogenate to scavenge free radicals implies that brain damage can be induced by free radicals since they are known to react virtually with any type of molecule such as nucleic acids, membrane lipids, and proteins in the brain.
Overall, these studies indicate that free radicals are possibly involved in the pathogenesis of neuron death in AD.
We conclude that oxygen and glucose deprivation causes a moderate increase in the formation of free radicals in NT2-N neurons that can be inhibited by antioxidants and by blocking of the N-methyl-d-aspartate–glutamate receptor.
These findings suggested that free radicals can be produced during brain damage induced by seizures.
Removal of pathologically produced free radicals is therefore a viable approach to neuroprotection.
Moreover, evidence was obtained that when, in the living organism, free radicals are not neutralized by systems of biochemical defences, many pathological conditions develop.
Generation of free radicals in vivo also may be the result of exposure to certain chemical agents present in the environment.
This study is the first report demonstrating noninvasively the presence of free radicals in vivo coming from food.

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