CO–metal interaction: vital signaling from a lethal gas

The past few years have witnessed intense research into the biological significance of carbon monoxide (CO) as an essential signaling mediator in cells and tissues. To transduce the signal properly, CO must react selectively with functional and structural proteins containing moieties that show preferred reactivity towards this gaseous molecule. This selectivity is exemplified by the interaction of CO with iron- and heme-dependent proteins, although systems containing other transition metals can potentially become a preferential target for CO. Notably, transition metal carbonyls, which carry and liberate CO, are also emerging as a pharmacological tool to mimic the bioactivity of endogenously generated CO. Thus, exploring how CO binding to metal complexes is translated into a cytoprotective function is a challenging task and might open up opportunities for therapeutic applications based on CO delivery.