The water-soluble ferriheme model Fe(III)(TPPS) mediates oxygen atom transfer from inorganic nitrite to a water-soluble phosphine (tppts), dimethyl sulfide, and the biological thiols cysteine (CysSH) and glutathione (GSH). The products with the latter reductant are the respective sulfenic acids CysS(O)H and GS(O)H, although these reactive intermediates are rapidly trapped by reaction with excess thiol. The nitrosyl complex Fe(II)(TPPS)(NO) is the dominant iron species while excess substrate is present. However, in slightly acidic media (pH ≈ 6), the system does not terminate at this very stable ferrous nitrosyl. Instead, it displays a matrix of redox transformations linking spontaneous regeneration of Fe(III)(TPPS) to the formation of both N2O and NO. Electrochemical sensor and trapping experiments demonstrate that HNO (nitroxyl) is formed, at least when tppts is the reductant. HNO is the likely predecessor of the N2O. A key pathway to NO formation is nitrite reduction by Fe(II)(TPPS), and the kinetics of this iron-mediated transformation are described. Given that inorganic nitrite has protective roles during ischemia/reperfusion (I/R) injury to organs, attributed in part to NO formation, and that HNO may also reduce net damage from I/R, the present studies are relevant to potential mechanisms of such nitrite protection.