Chapter 30 Nitric oxide: cellular regulation and neuronal injury

摘要: Publisher Summary A variety of mechanisms have been proposed for NO neurotoxicity, including inhibition mitochondrial enzymes such as cis-aconitase, the mitochondria1 electron transport chain, ribonucleotide reductase, DNA damage, mono-adenosine diphosphate (ADP)-ribosylation, and S-nitrosylation glyceraldehyde-3-phosphate dehydrogenase. Excessive stimulation N-methyl-D-aspartate (NMDA) by glutamate leads to excess production NO, which is toxic neurons under a experimental paradigms pathological conditions. When excessive amounts are formed in response actions excitatory neurotransmitter, glutamate, acting at NMDA receptors, mediates components neuronal killing toxicity via may account neural damage associated with acquired immunodeficiency syndrome (AIDS) dementia well cerebral infarction. Strategies aimed decreasing formation or identifying targets NO'S action clinical relevance development agents can prevent reverse these degenerative disorders.