ABSTRACT
Nitric oxide (NO) is a gaseous molecule produced from Nitric Oxide Synthases (NOS) enzyme. Three isoforms of NOS have been observed: endothelial NOS (eNOS), inducible NOS (iNOS) and neuronal NOS (nNOS). All three of these isoforms are expressed in liver in varying spatial and temporal ways. In liver, both nNOS and eNOS maintain homeostasis. Whereas iNOS is not expressed constitutively in liver, but rather is expressed in most liver cell types given the appropriate stimulatory conditions. Conflicting results have been observed on the behaviour and possible roles of the NO in several models of ischemia/ reperfusion injury during liver transplantation. Indeed, endogenous NO production has been associated with either protective or cytotoxic effects. Thus some, not all studies suggest that although eNOSderived NO production is protective in ischemia/reperfusion, iNOS derived NO production may contribute to ischemia/ reperfusion injury. This review article focuses on possible role of NO in liver transplantation.