ABSTRACT
From neurotransmission to cardiovascular vasodilation to microbial killing, ni tric oxide is involved in a diverse array of physiological and pathophysiological functions. In mammals including humans, NO is produced by three isoforms of nitric oxide synthases (NOS). The constitutive ones are known as NOSĮ (nNOS or ncNOS, neuronal constitutive) and NOS3 (eNOS or ecNOS, endothelial con stitutive); and the inducible one as NOS2 (iNOS, inducible). A variety of cell types produce NO. The level of NO generation is low for NOSĮ and NOS3, but high for NOS2. High NO output is engaged during inflammation and infection (1-3). However, NO is a double-edged sword (4). Whereas NO is a regulator of a multitude of cellular functions, its overproduction in chronic inflammation may be detrimental. Excess NO can react with DNA, leading to mutations and even tually carcinogenesis (5,6). Hence, under specified pathophysiological conditions, selective modulation of the NO pathway is desirable.
