The co-application effects of fullerene and ascorbic acid on UV-B irradiated mouse skin.
The role of fullerene as a pro-oxidant or anti-oxidant in Ultraviolet B ray (UV-B)-induced disorders in mouse skin was investigated. Fullerene gave no photo-toxic effect to UV-B-irradiated mouse skin. Since erythema was concentrated at the pore circumference in a UV-B irradiation experiment in mouse skin, the sebaceous gland pairs was strongly implicated as a site for the generation of reactive oxygen species (ROS). In a histological evaluation of the skin stained with CH(3)MDFDA (ROS index) and YO-Pro-1 (apoptosis index), the fluorescence intensity of a sebaceous gland significantly increased with UV-B irradiation. With the application of fullerene to UV-irradiated mouse skin, no toxicity was recognized in comparison with the control, and erythema, the ROS index, and the apoptosis index decrease with the application of fullerene. Ascorbyl radical (AA*) increased with the application of ascorbate (AA) to UV-B-irradiated mouse skin, and AA* decreased with the application of fullerene. The co-application of AA and fullerene, which suppressed AA* in vitro, significantly suppressed erythema, and also suppressed both the ROS index and apoptosis index in mouse skin after UV-B irradiation. In both mouse skin at 48 h after UV-B irradiation and in an attempt to reproduce this phenomenon artificially in vitro, a similar high AA* peak (AA*/H*>4) was observed in electron spin resonance (ESR) charts. The binding of fullerene with AA impairs the Fenton reaction between AA and Fe-protein based on the observation of ascorbate-specific UV absorption and a linear equation for the calibration curve. Therefore, fullerene may impair the intercalation of AA to a heme pocket by binding with AA. These results suggest that the co-application of AA and fullerene is effective against oxidative skin damage caused by UV-B irradiation, and the development of an AA* inhibitor such as fullerene should be useful for reducing organ damage associated with Fe-protein oxidation.
Ito
Shinobu
S
Tokyo Women's Medical University, Institute of Advanced Biomedical Engineering and Science, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, Japan.
Itoga
Kazuyoshi
K
Yamato
Masayuki
M
Akamatsu
Hirohiko
H
Okano
Teruo
T
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D001205:Ascorbic Acid / Q000627:therapeutic use*; D003683:Dehydroascorbic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D004359:Drug Therapy, Combination; D037741:Fullerenes / Q000627:therapeutic use*; D006861:Hydrogen Peroxide; D007501:Iron; D008297:Male; D051379:Mice; D010787:Photosensitivity Disorders / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012867:Skin / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D014466:Ultraviolet Rays
D000975:Antioxidants; C045076:Fenton's reagent; D037741:Fullerenes; D017382:Reactive Oxygen Species; C000820:semidehydroascorbic acid; D006861:Hydrogen Peroxide; D007501:Iron; D001205:Ascorbic Acid; D003683:Dehydroascorbic Acid