Formation of dinitrosyl iron complexes (DNICs), which can be described by general formula Fe(NO)2(L)2, where L is carbonyl-, nitrosyl- or imino- complexing ligand, was observed in many kinds of living organisms, in a wide spectrum of physiological conditions associated with inflammation, ischemia/reperfusion and cancer. Accumulation of DNICs coincides with intensified production of nitric oxide in macrophages, neurons, endothelial cells, Langerhans' cells and hepatocytes. Low-molecular thiol-containing DNICs (DNIC-(RS)2) show vasodilatory action and they are proposed to play a role of nitric oxide transducers and stabilizers. DNICs have been shown to modulate redox potential of the cell via inhibition of glutathione-dependent enzymes, such as glutathione reductase, S-transferase and peroxidase. Although there is a convincing experimental evidence for their NO and NO+ donating function, the nature of DNICs formed in biological systems, their stability and biological role is still a matter of discussion.