Nitric oxide metabolism after traumatic brain injury

Abstract

Nitric oxide (NO) is a cell membrane-permeable free radical gas and is the smallest known biologically active molecule. NO can be produced by nearly all tissues of the body. NO is synthesized from the semi-essential amino acid, L-arginine, by the enzyme, nitric oxide synthase (NOS). Three isoforms of NOS exist: Endothelial (eNOS), neuronal (nNOS), and inducible (iNOS). Agents that selectively inhibit the individual isoforms of NOS, as well as transgenic mice that are deficient in each of the isoforms of NOS, have played important roles in understanding the normal functions of NO and the changes in NO metabolism that occur with neurological disorders like traumatic brain injury (TBI) [1]. © 2007 Springer Science + Business Media Inc.