Catalyzes the oxidative cleavage of heme at the alpha-methene bridge carbon, released as carbon monoxide (CO), to generate biliverdin IXalpha, while releasing the central heme iron chelate as ferrous iron (By similarity) Affords protection against programmed cell death and this cytoprotective effect relies on its ability to catabolize free heme and prevent it from sensitizing cells to undergo apoptosis (By similarity). Catalyzes the oxidative cleavage of heme at the alpha-methene bridge carbon, released as carbon monoxide (CO), to generate biliverdin IXalpha, while releasing the central heme iron chelate as ferrous iron. heme b + 3 O2 + 3 reduced [NADPH--hemoprotein reductase] = biliverdin IXalpha + CO + Fe(2+) + H(+) + 3 H2O + 3 oxidized [NADPH--hemoprotein reductase] Induced by its substrate heme, CdCl2, sodium arsenite and 12-O-tetradecanoyl-phorbol-13-acetate (PubMed:3409220, PubMed:8288554). It is also induced in macrophages, liver and the lungs upon infection with M.tuberculosis (at protein level). Data is conflicting as to whether macrophage induction is independent of the nitric oxide (NO) signaling pathway (PubMed:18400743), or dependent on NO (PubMed:18474359). A soluble form arises by proteolytic removal of the membrane anchor. Belongs to the heme oxygenase family.