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Free Radicals and the Pathogenesis of Neuronal Death: Cooperative Role of Excitatory Amino Acids

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Free Radicals in Diagnostic Medicine

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 366))

Abstract

The potential role of oxygen-derived free radicals in the pathogenesis of neuropsychiatric diseases has been thoroughly discussed in the past few years1, 2, 3. The neurotoxic consequences of superoxide anion, hydrogen peroxide and hydroxyl radical formation have been described, as well as their relevance to abnormal conditions of the central nervous system, such as hyperoxia, hemorrhage, trauma, and aging. A separate line of investigation over the last ten years has established that excessive release of the excitatory neurotransmitter glutamate and sustained activation of glutamate receptors may also be responsible for neuronal degeneration associated with epilepsy, cerebral ischemia, hypoglycemia and other neurodegenerative diseases4, 5, 6. It is now emerging that free radical formation and glutamate receptor activation may act in concert, cooperating in the genesis and propagation of neuronal damage7, 8, 9. The goal of this report is to examine the potential relationship between these two pathogenic events in neurological disease, with particular stress on mechanisms underlying post-ischemic brain damage.

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Pellegrini-Giampietro, D.E. (1994). Free Radicals and the Pathogenesis of Neuronal Death: Cooperative Role of Excitatory Amino Acids. In: Armstrong, D. (eds) Free Radicals in Diagnostic Medicine. Advances in Experimental Medicine and Biology, vol 366. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1833-4_5

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  • DOI: https://doi.org/10.1007/978-1-4615-1833-4_5

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