Publisher Summary A variety of mechanisms have been proposed for NO neurotoxicity,
including inhibition of mitochondrial enzymes such as cis-aconitase, inhibition of the
mitochondria1 electron transport chain, inhibition of ribonucleotide reductase, DNA damage,
mono-adenosine diphosphate (ADP)-ribosylation, and S-nitrosylation of glyceraldehyde-3-
phosphate dehydrogenase. Excessive stimulation of N-methyl-D-aspartate (NMDA) by
glutamate leads to excess production of NO, which is toxic to neurons under a variety of …