AHR and porphyria: In DDC-treated liver, AhR ligands are endogenously produced either in the course of oxidative stress (oxidation products of polyunsaturated fatty acids or amino acids, like tryptophan36) or from bilirubin and other heme derivatives37 as a consequence of porphyria, and increased degradation of heme resulting from upregulation and mitochondrial translocation of HO-111; (ii) stabilization of hypoxia-inducible factors by DDC-induced oxidative stress38,39.