Abstract
Nitrite has been shown in the past decade to be an important source of nitric oxide that acts as a vasodilator and intrinsic signaling molecule. Numerous studies have proved that nitrite can be reduced in vivo, either non-enzymatically or enzymatically, in reactions catalyzed by xanthine oxidase, deoxyhaemoglobin, deoxymyoglobin, cytochrome c, or by thiol and metal-center-assisted processes inside the cell. The mechanism of the last process has recently been studied in detail, and has demonstrated that thiols (cysteine and gluthathione) stimulate water-soluble Fe-porphyrins to have nitrite reductase activity through an oxygen atom transfer (OAT)mechanism (Scheme 1) that leads to increased
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