iNOS Expression in Oral and Gastrointestinal Tract Mucosa

Abstract

It is known that the overproduction of nitric oxide (NO) by nitric oxide synthase (NOS) occurs during the progression of various inflammatory diseases in intestinal tract. NOS inhibitors or inducible nitric oxide synthase (iNOS) gene expression inhibitors should be considered as potential anti-inflammatory agents, as NO synthesized by iNOS is related to various pathophysiological processes including inflammation. In order to understand the relationship between iNOS and pathological reactions such as the inflammatory process and malign transformation clearly, the existence and amount of constitutive expression should be determined. It is crucial to comprehend the harmful and protective amounts of iNOS expressions in order to clarify the relationship between iNOS and pathological processes. Evidently, only after this inspection is it possible to utilize iNOS as a marker and treatment instrument during the diagnosis and treatment of malign transformation and the inflammatory process.

Quantitative and qualitative evaluation of iNOS expression in turbot (Psetta maxima) infected with Enteromyxum scophthalmi

“…The stained leukocytes morphologically corresponded to macrophages or granulocytes and the presence of the enzyme in these phagocytes would be similar to that described in other species [10,19]. The expression of iNOS in vascular structures has been reported as the up-regulation of the enzyme in the vascular smooth muscle which causes vascular relaxation, vasodilatation and then congestion due to the infection or related to chronic pathological processes [27,28].…”

“…The goblet cells of the gut sections closest to the environment differentially may express molecules related to nonspecific host defence, such as acidic mucins in the oesophagus and lysozyme in the hindgut (authors' unpublished results). A preferential location of iNOS in the apical pole of enterocytes has been described [10], as well as immunostaining for eNOS in goblet cells of the nasal mucosa, which has been demonstrated to participate in the liberation of NO during inflammatory processes [33]. Since the presence of an isoform of NOS was demonstrated in goblet cells, the expression of iNOS in turbot goblet cells in areas close to the anus of the digestive tract would suppose an active participation of this cell type in the liberation of NO during inflammatory responses in the mid and hindgut due to their proximity to the environment.…”

Dietary fat sensing via fatty acid oxidation in enterocytes: possible role in the control of eating

“…Another potential link between FAO and NO is that pharmacologic activation of AMPK, which increases FAO, markedly inhibits the inducible form of NO synthase and, hence, decreases NO production (125). AMPK (164) and inducible form of NO synthase (72) are present in enterocytes.…”

Polydatin, a natural precursor of resveratrol, induces cell cycle arrest and differentiation of human colorectal Caco-2 cell

“…Under these conditions, NO synthase II is induced in a variety of cells including the intestinal epithelium. NO synthase II, is capable of generating high local intracellular and extracellular concentrations of NO [12-14]. As part of the inflammatory process or sepsis, activated inflammatory cells generated large amounts of superoxide anions (O 2 - ).…”