Abstract
Nitric oxide (NO) was first found as an endothelium-derived relaxing factor, but has also been shown to affect cerebral blood flow and cell signal transduction. It is important that NO itself is not so toxic or reactive in vivo, and that rapid reaction with superoxide forms a more powerful biological species, peroxynitrite. It is suggested that reaction of peroxynitrite with superoxide dismutase (SOD) nitrates protein tyrosine, so facilitating cell degeneration after ischemia. This mechanism could also explain the reason for motor neurron death in farmilial amyotrophic lateral sclerosis, in which SOD point mutations were recently found.
