[Paradoxes of cerebral oxidative metabolism]

The free radical forms of oxygen resulting from disorders in brain blood supply and accumulated by subsequent reperfusion modify neuron metabolism in two different ways. On the one hand, free oxygen radicals activate the breakdown and destruction of neuronal membranes caused by ischemia and provide the oxidative attack at the key neuronal receptors and enzymes involved in excitation. On the other hand, they can play a role of specific messengers regulating vasodilation and adjusting neurons to the changed conditions of functioning. As a consequence, the antioxidant protection of the brain provided by hydrophobic antioxidants characterized by a lag period appears to be less effective than the protective effect of natural hydrophilic antioxidants having a direct action.