Abstract
Nitric oxide (NO) is generated from L-arginine by the enzyme NO synthase (NOS) [1]. NO production requires many cofactors, including nicotinamide dinucleotide phosphate (NADPH), flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD) and tetrahydrobiopterin [1, 2]. Three genes encoding NO synthases are expressed as enzymes in mammals [3, 4]. These enzymes are denoted either by their historical order of cloning or by the cell type from which their cDNA was first cloned. Thus, the human genes encoding neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS) are termed NOS1, NOS2, and NOS3, respectively. Of the three major NOS isoforms, eNOS and nNOS are calcium-dependent enzymes, and are generally but not invariably expressed constitutively and denoted therefore cNOS. NOS2 was named “iNOS” to connote its independence of elevated intracellular Ca2+the distingushing biochemical feature primarily responsible for conferring the capacity of this isoform for more sustained catalysis than typically exercised either by nNOS or eNOS. Because iNOS is expressed in most cells only after induction by immunologic and inflammatory stimuly, the “i” doubles for “inducible”. cNOS has been localised in vascular endothelium (eNOS), platelets, and neurons (nNOS) of the central nervous system [1].
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Haddad, EB. (2000). Role of Nitric Oxide in Airway Inflammation. In: Belvisi, M.G., Mitchell, J.A. (eds) Nitric Oxide in Pulmonary Processes. Respiratory Pharmacology and Pharmacotherapy. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8474-7_8
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