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CJ Walton, S Sadda, R Grebe, L Grebe, S Arai, E de Juan Jr; The Protective Effect of Genistein on Blue-Light Damaged Retinal Tissue of Age-Accelerated Mice at 28 Weeks . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3736.
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Purpose: To determine the effect of orally administered genistein on the blue light damage of retina within the senescence-accelerated mouse(SAM)at 28 weeks of exposure Methods: The blue light exposure was set up according to Gottsch et al (Arch Ophthalmol 1993;111:126). Forty-eight SAM P8 mice were divided into four groups. Within each group, the mice were exposed to continuous blue light. One group received a normal, genistein-free diet, one a fatty diet, one a fat+genistein diet, and one a genistein-rich diet. The mice were treated in this fashion for 28 weeks, beginning 4 weeks after birth. The effect of genistein was evaluated using electron microscopy at this specific time. Results: After 28 weeks, using electron microscopy, P8 mice receiving constant blue light and a fatty diet showed a significant thickening of Bruch's membrane and an increase in RPE-deposits compared with the mice receiving the other diet groups. Those with the pure fat diet showed atrophy of the choriocapillaris and a Bruch's membrane invasion by the endothelial cells, not readily seen with the other mice. In addition, a 30% reduction in the density of the photoreceptor outer segments and a 15% breakdown of cellular structure within the outer nuclear layer was evident compared with the mice receiving the other diets. The mice receiving the fat+genistein and the normal diets showed similar patterns of degeneration involving Bruch's membrane, the RPE, and the choriocapillaris. There was markedly less thickening of Bruch's membrane, fewer RPE deposits, and less invasion of Bruch's by the choriocapillaris compared with the mice receiving the fatty diet. In the P8 mice with pure genistein treatment, the thickening of Bruch's membrane was significantly inhibited with fewer RPE-deposits compared with the other groups. A sharp demarcation between Bruch's and the choriocapillaris was evident with a significant increase in photoreceptor outer segment density versus the other diet groups. Conclusions: Our results indicate that diet plays a major role in the progression of retinal damage induced by blue light exposure. A diet high in fat seems to accelerate this damage, particularly within Bruch's membrane, the RPE, and the choriocapillaris. Alternately, genistein seems to significantly slow the retinal regression found with blue light exposure and possibly has a protective effect on the retinal degeneration seen with the aging process.
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