Abstract

The lipophilic antioxidant U-18 from the class of hindered phenols prevents the destruction of cultured hippocampal neurons during hypoxia and also in the posthypoxic reoxygenation period, apparently by being stably incorporated into their phospholipid membranes and by safeguarding these from free-radical damage in the course of reoxygenation. On the other hand, the protection afforded to the cultured hippocampal neurons by superoxide dismutase is probably due to its ability to interfere with the posthypoxic neuron-degrading processes mediated through hyperproduction of superoxide radicals in the neuronal cytoplasm.

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