Hypoxia potentiates ultraviolet A-induced riboflavin cytotoxicity.
Flavins are thought to be important chromophores for chronic photo-induced skin injury, but the mechanism is not well known. We have reported that the primary cytotoxicity remaining in ultraviolet A-irradiated riboflavin solution is attributable to hydrogen peroxide. Because the dermis is more hypoxic than the atmosphere, we investigated the cytotoxicity of riboflavin solution during and after ultraviolet A irradiation under hypoxia. Riboflavin solution showed stronger cytotoxicity during irradiation under hypoxia than under air. Riboflavin solution that had been irradiated under hypoxia at lower ultraviolet A doses showed stronger cytotoxicity and contained more hydrogen peroxide than solution irradiated under air at the same doses. At higher ultraviolet A doses, however, the cytotoxicity and hydrogen peroxide quantity were similar in riboflavin solutions irradiated under different oxygen conditions. The effect of a singlet oxygen quencher, sodium azide, on the induction of cytotoxicity and production of hydrogen peroxide by ultraviolet A irradiation of riboflavin solution was examined. The presence of sodium azide in the solution during ultraviolet A irradiation suppressed the cytotoxicity and hydrogen peroxide production to similar levels at various ultraviolet A doses regardless of oxygen conditions. At the maximum suppression by sodium azide, hydrogen peroxide production decreased to 10% of the unsuppressed production. About 40% of the oxygen molecules of hydrogen peroxide produced was thought to be derived from oxygen dissolved in the riboflavin solution.
Minami
H
H
Department of Dermatology, Osaka University School of Medicine, Suita, Japan.
Sato
K
K
Maeda
T
T
Taguchi
H
H
Yoshikawa
K
K
Kosaka
H
H
Shiga
T
T
Tsuji
T
T
D002460:Cell Line; D004578:Electron Spin Resonance Spectroscopy; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects / Q000528:radiation effects; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D017665:Hydroxyl Radical / Q000378:metabolism; D000860:Hypoxia / Q000503:physiopathology*; D010100:Oxygen / Q000378:metabolism; D017319:Photosensitizing Agents / Q000378:metabolism / Q000633:toxicity*; D012256:Riboflavin / Q000378:metabolism / Q000633:toxicity*; D019810:Sodium Azide / Q000494:pharmacology; D012996:Solutions / Q000737:chemistry / Q000378:metabolism / Q000528:radiation effects; D014466:Ultraviolet Rays
D004791:Enzyme Inhibitors; D017319:Photosensitizing Agents; D012996:Solutions; D017665:Hydroxyl Radical; D019810:Sodium Azide; D006861:Hydrogen Peroxide; D010100:Oxygen; D012256:Riboflavin