The development of new retinal oxidative stress market and the effects of vitamin E intensive care against retinal light damage

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Maternal animals and pups of α-Tocopherol transfer protein (α-TTP) null mice were fed a vitamin E (VE) deficient diet for 4- or 18-months [VE (-) group]. Wild type. C57BL/6 mice were fed with 0.002 % α-tocopherol-supplemented diet [VE (+) group]. In retinas from 4-month-old VE (-) animals, the level of α-tocopherol, as measured by high performance liquid chromatography, was 71-fold lower than VE (+) group and γ-tocopherol was not detected, thus VE (-) group yielded more severe VE deficiency than ever reported. By gas chromatography analysis, n-3 pulyunsaturated fatty acids decreased (0.3- to 0.9-fold) in VE (-) mice, whereas other classes of fatty acids were unchanged or increased. When 18-month-old animals were compared to 4-month-old animals, levels of hydroxyoctadecadienoic acid and 8-iso-prostaglandin F^<2α>, biomarkers for lipid peroxidation, assessed by gas chromatography-mass spectrometry (GC-MS) were increased in retina and retinal pigment epithelium (RPE) from both VE (-) and (+) groups, whereas these age-related increases were more remarkable in VE (-) groups (2.6- to 43.5-fold) than VE (+) groups (0.8- to 8.7-fold). At 18-months of age, by light microscopy, number of outer nuclear layer (ONL) nuclei was 17 % lower in VE (-) than (+) groups (p<0.05). By electron microscopy, larger amounts of fibrous tissues between ONL nuclei, greatly expanded rod outer segment disks, and larger numbers of inclusion bodies in RPE (p<0.05) were observed in VE (-) group. By fluorescence microscopy, autofluorescence was increased in the RPE layer of VE (-) group. Severe deficiency of VE enhances increased lipid peroxidation and results in structural changes during aging in retina, indicating anti-aging roles of vitamin E.