The transport of NO into and out of cells is of great importance, particularly as it relates to its messenger and cytotoxic effector functions. We have demonstrated that NO can stimulate cellular 59Fe and GSH release by a mechanism that is mediated by MRP1 (Fig. 6) . This may be important for a number of reasons. For instance, the release of DNICs from the cell by a specific transport process could be important for intercellular responses to this messenger molecule and may impart NO with a greater half-life. In fact, a number of investigations have reported that DNICs (e.g. dinitrosyl-diglutathionyl-Fe complex) are natural carriers and storage forms of NO that possess a greater half-life than NO alone [93-97]. Considering this, it is relevant to note that DNICs have been found in animal tissues, human
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