Lutein, a xanthophyll of a
carotenoid, is anticipated as a therapeutic product to prevent human
eye diseases. However, its
biological mechanism is still unclear. Here, we show the molecular mechanism of
lutein's effect to reduce photodamage of the retina. We analyzed the light-exposed retinas of Balb/c mice given
lutein-supplemented or normal diet. Visual function was measured by electroretinogram, and histological changes were observed. Immunohistochemical and immunoblot analyses were performed to analyze molecular mechanism. The
reactive oxygen species induced in the retina was evaluated by
fluorescent probes. In the mice after light exposure, reduction of a-wave and b-wave amplitudes in electroretinogram, indicating
visual impairment, and thinning of the photoreceptor cell layer owing to apoptosis were both attenuated by
lutein diet. Interestingly, γ-H2AX, a marker for double-strand breaks (DSBs) in
DNA, was up-regulated in the photoreceptor cells after light exposure, but this increase was attenuated by
lutein diet, suggesting that DSBs caused by photodamage contributed to the photoreceptor cell death and that this change was suppressed by
lutein. Moreover, the expression of eyes absent (EYA), which promotes DNA repair and cell survival, was significantly up-regulated with
lutein diet in the light-exposed retina. Therefore,
lutein induced EYA for DNA repair, which could suppress DNA damage and photoreceptor cell apoptosis.
Lutein reduced light-induced oxidative stress in the retina, which might contribute to promote DNA repair. The
lutein-supplemented diet attenuated light-induced
visual impairment by protecting the photoreceptor cells'
DNA.