Lutein and Oxidative Stress-Mediated Retinal Neurodegeneration in Diabetes

Although many details remain elusive, recent progress in molecular biology has elucidated the underlying mechanisms of many disease pathogeneses, including some fundamental concepts. One such concept is that oxidative stress is involved in the age-related progression of diseases, as observed in diabetic complications and neurodegenerative diseases. Concordantly, oxidative stress accumulates with time, and can eventually overcome the biological defense systems. Therefore, the progression of the diseases might be prevented or slowed by suppressing oxidative stress. Here we focus on lutein, a plant-derived carotenoid and food factor that can act as an antioxidant in the mammalian retina. In an animal model of diabetes, the continuous intake of lutein suppresses the diabetes-related reduction of synaptophysin protein and brain-derived neurotrophic factor in the retina, and the subsequent visual function impairment. This mechanism overlaps with the renin-angiotensin system. Here we review the involvement of oxidative stress in diabetes-associated retinal neurodegeneration and discuss lutein's neuroprotective effects.