Poster (download) Darya V. Telegina1, Oyuna S. Kozhevnikova2, Anzhela Z. Fursova31ICG SB RAS, Novosibirsk, Russia, telegina@bionet.nsc.ru2ICG SB RAS, Novosibirsk, Russia, oidopova@bionet.nsc.ru3ICG SB RAS, Novosibirsk, Russia, anzhellafursova@yandex.ru Melatonin and antioxidant SkQ1 act like mitochondria-targeted antioxidants, which concentrate in mitochondria at relatively high levels and they may prevent mitochondrial damage during retinal aging and development of age-related retinal disease such as age-related macular degeneration (AMD). However, detailed effects of melatonin and SkQ1 on the biochemical mechanisms underlying therapeutic effect of these drugs during retinal aging and AMD progression remain unclear.В  Using Wistar rats with normal aging process and senescence-accelerated OXYS rats, which spontaneously develop a phenotype similar to human age-related disorders including AMD-like retinopathy, we found that treatment of SkQ1 and melatonin decreased the incidence and severity of retinopathy in OXYS rats. In Wistar rats, which do not naturally develop retinopathy, ophthalmoscopic inspections did not reveal pathological alterations in the retina of melatonin and SkQ1-treated rats. SkQ1 decreased p62/SQSTM1 protein but not mRNA levels in both OXYS and Wistar rat\’s retinas as compared of control rats. We observed reduced level of VDAC1 and increased level of glutaminase by long-term treatment of melatonin and SkQ1 in retina of Wistar rats but not OXYS rats. Taken together, our data indicated that long-term treatment of melatonin and mitochondria-targeted antioxidant SkQ1 may retard an age-related decline in the adaptability of retinal cells and may be considered as a strategy to slow down AMD. At the same time effects of melatonin and SkQ1 on molecular events may be different depending on genotype and disease.

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