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[DOI] [PMC free article] [PubMed] [Google Scholar] 90.Zhu R, Baker S S, Moylan C A et al

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There is also evidence that oxidative stress enhances TNF-alpha neurotoxicity and that antioxidants reduce this toxicity.[238] Nitric oxide Elevations in NO with brain injury are also known to occur.[46,77,262] A number of studies have shown that NO itself is neuroprotective, but in the face of high free radical generation, NO combines with superoxide to form the very destructive peroxynitrite radical, which has a specific damaging effect on mitochondrial function.[212] NO also competes with oxygen for cytochrome oxidase within mitochondria, reducing ATP generation and triggering glutamate release.[26] Bal-Price and Brown have shown that NO killing of neurons was completely prevented by blocking glutamate receptors.[7] Reducing mitochondrial energy production has been shown to greatly increase the neurodestructive effects of excitotoxins.[88,168,169] The metabotropic glutamate receptors play a significant role in this process, since they can either enhance excitotoxicity or reduce it, depending on the specific subtype of metabotropic receptors activated or suppressed.[170] Mechanisms of brain protection Of significant importance is the role played by the protective mechanisms utilized by the brain to contain excess extraneuronal excitatory amino acids