Furocoumarins photosensitize biomolecules to 320- to 400-nm UV by way of Type I (sensitizer-substrate) and Type II (sensitizer-oxygen) mechanisms. The Type I reactions with DNA are mediated by ground state complexes. Covalent monoadducts of the furocoumarin with pyrimidines are formed in the first photochemical step. A fraction of the monoadducts of difunctional furocoumarins are converted to interstrand cross-links in a second photochemical step, as controlled by the type of monoadduct site and the spectral distribution of the radiation. Certain furocoumarins generate singlet molecular oxygen by energy transfer from the furocoumarin triplet state. The photosensitized inactivation of enzymes involves a Type II mechanism mediated by singlet oxygen. Singlet oxygen reacts with 8-methoxypsoralen to form long-lived products, which have been implicated in the formation of covalent photoconjugates with serum albumin and other proteins and peroxidation of unsaturated lipids. The available information about furocoumarin-photosensitized inactivation of microorganisms indicates that DNA monoadducts are removed by an efficient excision repair process, and DNA cross-links are removed by a more complex, error-prone process, both of which are under genetic control. The significantly higher sensitivity of microorganisms to difunctional furocoumarins has been identified with the formation of cross-links. Both monoadducts and cross-links induce mutations in microorganisms, with a strong dependence on the specific furocoumarin structure, the strain, and the type of mutation.