The primary cytotoxicity in ultraviolet-a-irradiated riboflavin solution is derived from hydrogen peroxide.

The cytotoxic action of near-ultraviolet (UVA) radiation on cultured mammalian cells is dependent upon oxygen, suggesting that reactive oxygen species are involved in the cellular action of the radiation. Flavins are thought to be an important chromophore for photo-induced skin injury. Irradiation of riboflavin with UVA radiation is known to produce singlet oxygen, superoxide anions, and triplet-state riboflavin radicals, which, however, are immediately quenched by many constituents of the human skin. If the chemical produces a long-lived reactive oxygen species, hydrogen peroxide (H2O2), after UVA radiation, its deleterious effect is not limited to its generation site. Thus, we investigated whether H2O2, is produced in UVA-irradiated riboflavin solution and whether it plays an important role in the cytotoxic action of the solution. The solution showed a marked cytotoxic effect when placed on human fibroblasts, and cytotoxicity was retained in the solution for at least 40 min after radiation. Most of the toxicity appeared to be derived from H2O2 produced in the solution, because the solution lost its cytotoxicity as a result of catalase treatment, and the resultant restoration of survival was almost complete. Under our conditions, two molecules of riboflavin were calculated to produce one molecule of H2O2 after UVA radiation.