Nitrite says NO to ischemia/reperfusion injury

Nitrite is a simple inorganic anion that is the end product of nitric oxide (NO) oxidation, and previously thought to have only limited biological activity. In a study appearing online on April 14 in advance of the print publication of the May issue of the Journal of Clinical Investigation, David Lefer and colleagues from Louisiana State University Health Sciences Center show that nitrite is a potent inhibitor of ischemia-reperfusion (I/R) injury in the liver and heart.

The researchers showed that nitrite therapy conferred a dose-dependent cell protective effect in mouse models of I/R injury, limiting cell death and preserving organ function. These effects are NO-dependent. The data demonstrate that nitrite could be used therapeutically for I/R disease, as it is already known that nitrite is safe, and it is an approved treatment for cyanide poisoning.

Nitrite therapy could potentially be used to prevent organ dysfunction following I/R injury to the heart or vasculature resulting from surgery or transplantation. Nitrite may also serve an endogenous protective mechanism that protects cells from severe stress.

TITLE: Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver

AUTHOR CONTACT:
David Lefer
LSU Health Sciences Center, Shreveport, LA USA
Phone: 318-675-6974; Fax: 318-675-4217; E-mail: dlefer@lsuhsc.edu

View the PDF of this article at: https://www.the-jci.org/article.php?id=22493

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Journal of Clinical Investigation
14-Apr-2005