Until now, relatively few studies have addressed the role of HO-1/CO in pulmonary medicine. Several investigators have focused on the diagnostic application of the HO-1/CO system, by measuring exhaled CO (E-CO) in various pathological pulmonary conditions, such as asthma or chronic obstructive pulmonary disease (COPD) [7] . In another experimental approach, investigators have examined the expression of HO-1 in lung tissue from healthy or diseased subjects [8, 9] . This review will highlight the actions of HO-1/CO in the context of heme degradation have antioxidant properties [18, 19] . The liberated heme iron undergoes detoxification either by extracellular efflux or by sequestration into ferritin, an intracellular iron-storage molecule with potential cytoprotective function [20] [21] [22] [23] . Of the three known isoforms of HO (HO-1, HO-2, and HO-3), only HO-1 responds to xenobiotic induction [24] [25] [26] [27] . Constitutively expressed in many tissues, HO-2 occurs at high levels in nervous and vascular tissues, and may respond to regulation by glucocorticoids [25, 28, 29] . HO-1 and HO-2 differ in genetic origin, in primary structure, in molecular weight, and in their substrate and kinetic parameters [25, 26] . HO-3 displays a high sequence homology with HO-2 but has little enzymatic activity [27] . This review will focus on the inducible, HO-1, form.