Blue light inhibits melanin synthesis in B16 melanoma 4A5 cells and skin pigmentation induced by ultraviolet B in guinea-pigs
Little has been known about the effects of visible light in mammalian cells. We recently found that blue light not only suppressed the growth of B16 melanoma cells in a time-dependent manner but also inhibited metastasis of the B16 melanoma cells to the lung. These findings suggest that exposure to blue light modifies the functions of B16 melanoma cells. The present study investigated the effects of blue light on B16 melanoma 4A5 cells and Weiser–Maple guinea-pigs to confirm the biological effect of blue light on melanin formation. Method:
The effect of red, green, and blue light on melanin synthesis in B16 melanoma 4A5 cells was measured. The back skin of brown Weiser–Maple guinea-pigs was exposed to ultraviolet B (UVB; 588 mJ/cm2 (0.7 mW/cm2× 14 min) three times a week for 2 weeks to induce melanin deposition. Thirty minutes after each UVB exposure, blue light was applied for 30 min. Pigmentation of the exposed areas of skin was checked once a week, and photographs of the skin were taken by digital camera. Observation was continued for 18 days after the final UVB exposure. Result:
Melanin synthesis in B16 melanoma 4A5 cells was selectively suppressed by blue light, but blue light did not induce decolorization of previously produced melanin. In the back skin of brown guinea-pigs, the brightness of the sites exposed to UVB began to decrease on the fifth day of the experiment, decreasing further from the 12th day to the 18th day after UVB exposure. The brightness of the sites exposed to UVB and blue light decreased in a manner similar during the UVB exposure, but remained relatively unchanged from the 12th day to the 30th day. Conclusion:
These results suggest that blue light suppresses melanin formation following repeated UVB exposure. Further investigation with various light such as blue light may lead to a new approach to the care of ultraviolet-affected skin such as hyperpigmentation.
Document Type: Research Article
Affiliations: 1: Otsuka Pharmaceutical Factory Inc., Muya-cho, Naruto, Tokushima, Japan, 2: Primate Ltd., Kyomachi, Kumamoto, Japan and 3: Department of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Kasumi, Minami-ku, Hiroshima, Japan
Publication date: 2004-04-01