Blue light-induced oxidative stress in live skin

被引:160
作者
Nakashima, Yuya [1 ]
Ohta, Shigeo [1 ]
Wolf, Alexander M. [1 ]
机构
[1] Nippon Med Sch, Grad Sch Med, Inst Dev & Aging Sci, Dept Biochem & Cell Biol,Nakahara Ku, 1-396 Kosugi, Kawasaki, Kanagawa 2118533, Japan
基金
日本学术振兴会;
关键词
Fluorescence; Photoaging; Aging; Redox; In vivo; GFP; Reactive oxygen species; Hydrogen peroxide; Superoxide; Singlet; AGE-RELATED MACULOPATHY; PHOTODYNAMIC THERAPY; SINGLET OXYGEN; NITRIC-OXIDE; IN-VITRO; GENERATION; MECHANISM; UVA; MITOCHONDRIA; IRRADIATION;
D O I
10.1016/j.freeradbiomed.2017.03.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Skin damage from exposure to sunlight induces aging-like changes in appearance and is attributed to the ultraviolet (UV) component of light. Photosensitized production of reactive oxygen species (ROS) by UVA light is widely accepted to contribute to skin damage and carcinogenesis, but visible light is thought not to do so. Using mice expressing redox-sensitive GFP to detect ROS, blue light could produce oxidative stress in live skin. Blue light induced oxidative stress preferentially in mitochondria, but green, red, far red or infrared light did not. Blue light-induced oxidative stress was also detected in cultured human keratinocytes, but the per photon efficacy was only 25% of UVA in human keratinocyte mitochondria, compared to 68% of UVA in mouse skin. Skin autofluorescence was reduced by blue light, suggesting flavins are the photosensitizer. Exposing human skin to the blue light contained in sunlight depressed flavin autofluorescence, demonstrating that the visible component of sunlight has a physiologically significant effect on human skin. The ROS produced by blue light is probably superoxide, but not singlet oxygen. These results suggest that blue light contributes to skin aging similar to UVA.
引用
收藏
页码:300 / 310
页数:11
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