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- W41402948 abstract "Publisher Summary Several studies have shown that NOS enzyme-independent NO formation occurs in biological systems. In many disease states, such as ischemia or shock, where acidosis and marked hypoxia occur, this pathway becomes the major source of NO and the magnitude of NO generation can be much greater than that which would be formed by normal tissue concentrations of NOS. The substrate source of this NO formation is nitrite, rather than the NOS substrate and a number of pathways of nitrite reduction to NO are proposed, which include nitrite disproportionation, nitrite reduction by myoglobin, reduction by anoxic mitochondria, by xanthine oxidoreductase, by hemoglobin. Thus, these pathways may “substitute” NO production from NOS in pathophysiological conditions, when NOS function is impaired and conditions might be favorable for nitrite reduction. From first glance, nitrite should display cytoprotective effect, since knockout of endothelial NOS leaves the hearts of mice more sensitive to ischemic damage. Protection should be similar to that observed with NO• donors. In models of infarction, nitrite has been reported to protect against ischemia—reperfusion damage in a way similar to NO donors. However, there is contradiction in literature. Studies in isolated rat hearts suggest that nitrite-derived cellular NO (or its derivatives) may be contributing to damage and, therefore, the effects of NO, derived from nitrite in myocardial injury are uncertain." @default.
- W41402948 created "2016-06-24" @default.
- W41402948 creator A5053625408 @default.
- W41402948 creator A5084568116 @default.
- W41402948 creator A5085032833 @default.
- W41402948 date "2007-01-01" @default.
- W41402948 modified "2023-09-23" @default.
- W41402948 title "Nitrite as NO donor in cells and tissues" @default.
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