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Am J Physiol Gastrointest Liver Physiol 276: G795-G799, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 4, G795-G799, April 1999

THEMES
Nitric Oxide
III. A molecular prelude to intestinal inflammation*

Mark J. S. Miller and Manuel Sandoval

Department of Pediatrics, Albany Medical College, Albany, New York 12208

Nitric oxide (NO) synthesis is markedly augmented in states of inflammation, largely due to the expression of inducible nitric oxide synthase (iNOS). Although NO has anti-inflammatory consequences under basal conditions, it remains enigmatic as to why NO displays proinflammatory characteristics in chronic inflammation. Either the anti-inflammatory actions are weak and of little consequence or, alternatively, other factors influence the role of NO in chronic inflammation. We propose that the answer to this enigma lies in the conversion of NO to other higher oxides of nitrogen (NO2, nitrogen dioxide; N2O3, dinitrogen trioxide; and ONOO-, peroxynitrite). Emerging therapeutic strategies may be independent of NO synthesis; e.g., antioxidants have no direct interaction with NO but attenuate the levels and activity of higher nitrogen oxides. Thus, whereas iNOS may be a marker for the proinflammatory actions of NO, the species that mediate tissue injury/dysfunction in inflammation are likely to be nitrogen oxides other than NO.

peroxynitrite; apoptosis; oxidant; cytokine

* Third in a series of invited articles on Nitric Oxide.




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