Abstract
In the retina, a number of degenerative diseases, including glaucoma, diabetic retinopathy, and age-related macular degeneration, may occur as a result of aging. Oxidative damage is believed to contribute to the pathogenesis of aging as well as to age-related retinal disease. Although physiological exercise has been shown to reduce oxidative stress in rats and mice, it is not known whether it has a similar effect in retinal tissues. The aim of this study was to evaluate retinal oxidative stress in naturally-aged mice. In addition, we evaluated the effects of aerobic training on retinal oxidative stress by immunohistochemically evaluating oxidative stress markers. A group of twelve-week-old male mice were not exercised (young control). Two groups of twenty-two-month-old male mice were created: an old control group and a treadmill exercise group. The old control group mice were not exercised. The treadmill exercise group mice ran on a treadmill (5 to 12 m/min, 30 to 60 min/day, 3 days/week for 12 weeks). The retinal thickness and number of cells in the ganglion cell layer of the naturally-aged mice were reduced compared to those in the young control mice. However, treadmill exercise reversed these morphological changes in the retinas. We evaluated retinal expression of carboxymethyllysine (CML), 8-hydroxy-2′-deoxyguanosine (8-OHdG) and nitrotyrosine. The retinas from the aged mice showed increased CML, 8-OHdG, and nitrotyrosine immunostaining intensities compared to young control mice. The exercise group exhibited significantly lower CML levels and nitro-oxidative stress than the old control group. These results suggest that regular exercise can reduce retinal oxidative stress and that physiological exercise may be distinctly advantageous in reducing retinal oxidative stress.
Highlights
Aging is a complex physiological phenomenon that is defined as a progressive loss of the efficacy of physiological and biochemical processes, which occurs until death [1]
In histopathological examination of hematoxylin and eosin (H&E)-stained retinal sections (Figure 1), we found that the retinal thicknesses of naturally aged mice (216.7 ± 14.8 μm) were slightly less than those in the young control mice (230.0 ± 10.0 μm, p < 0.05)
Histopathological study showed that structural alterations were significantly induced in the retinal cells of aged mice compared to young control mice
Summary
Aging is a complex physiological phenomenon that is defined as a progressive loss of the efficacy of physiological and biochemical processes, which occurs until death [1]. Retinal photoreceptor cells are among the most metabolically active cells, and they do not divide. These cells are sensitive to oxidative damage due to their increased oxygen consumption [5]. In retinal pigment epithelial cells, exposure to high doses of short wavelength visible light is cumulative, resulting in aging-associated retinal dysfunction, visual decline, or even vision loss, such as that associated with age-related macular degeneration, which is the leading cause of blindness among the elderly [6]. Retinal cells are exposed to a cumulative amount of oxidative and metabolic stress during the aging process. Increased oxidative stress and the accumulation of oxidative-modifications in key molecules induce the dysfunction of signaling pathways in various cells, thereby causing retinal cell injury [8]. There is still a lack of an efficacious remedy for these age-related retinal diseases due to incomplete understanding of the underlying mechanisms
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