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Several antitumour drugs have been isolated from natural products and many clinical trials are underway to evaluate their potential. There have been numerous reports about the antitumour effects of astaxanthin against several tumours but no studies into its effects against glioblastoma. Astaxanthin is a red pigment found in crustaceans and fish and is also synthesized in Haematococcus pluvialis; adonixanthin is an intermediate product of astaxanthin. It is known that both astaxanthin and adonixanthin possess radical scavenging activity and can confer a protective effect on several damages. In this study, we clarified the antitumour effects of astaxanthin and adonixanthin using glioblastoma models. Specifically, astaxanthin and adonixanthin showed an ability to suppress cell proliferation and migration in three types of glioblastoma cells. Furthermore, these compounds were confirmed to transfer to the brain in a murine model. In the murine orthotopic glioblastoma model, glioblastoma progression was suppressed by the oral administration of astaxanthin and adonixanthin at 10 and 30 mg/kg, respectively, for 10 days. These results suggest that both astaxanthin and adonixanthin have potential as treatments for glioblastoma.

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Non-exudative age-related macular degeneration (AMD) is an irreversibly progressive retinal degenerative disease characterized by dysfunction and loss of retinal pigment epithelium (RPE). It has been suggested that impaired phagocytosis of the RPE is involved in the progression of non-exudative AMD, but the mechanism is not fully clear. In this study, we investigated the effect of lipid droplet accumulation on RPE function. Compared to young mice, the expression of lipid droplet-associated proteins increased in the RPE-choroidal complex, and lipid droplet in the RPE was observed in aged pigmented mice (12-month-old). Repeated treatment of the photoreceptor outer segment against ARPE-19 resulted in lipid droplets in ARPE-19 cells in vitro. Oleic acid treatment for ARPE-19 cells to form intracellular lipid droplet reduced the POS uptake into the ARPE-19 cells without causing a decrease in cell viability. The suppression of the POS uptake by lipid droplet formation improved by inhibiting lipid droplet formation using triacsin C. Moreover, the amount of intracellular reactive oxygen species was suppressed by the triacsin C treatment. These results indicate that lipid droplet is involved in the RPE dysfunction, and inhibiting lipid droplet formation may be a target for preventing and treating non-exudative AMD.

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White light emitting diode (LED) lighting is being used more frequently for illumination in recent years. The coupling of blue with yellow emitting phosphors produces white LED light. Blue light has a short wavelength in the visible light spectrum and exerts a strong influence on photobiological functions. Cycling light exposure is necessary for the synchronizing the circadian rhythm. The exposure to white light at subjective nighttime induces cognitive impairment, depression, and anxiety by disturbing the circadian rhythm and increasing stress hormone. However, few studies have been performed at the subjective daytime. Thus, the aim of this study was to determine whether exposure to blue light from an LED at subjective daytime affects brain function. We irradiated C57BL/6J mice with 200 lux of blue LED light for 12 h/day for 6 weeks at the subjective daytime and performed Y-maze, object recognition, tail suspension, and open field tests. There was no significant difference between the exposed mice and control mice. Histological analysis of the retina showed that the blue light exposure did not alter the retinal thickness. We conclude that the exposure to blue LED light at subjective daytime does not affect the retinal morphology or brain function in pigmented mice.