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Renu Kowluru, Qing Zhong, Julia Santos, Mangayarkarasi ThandampallayamAjje, Douglas Putt, Dennis Gierhart; Potential beneficial effects of carotenoids on diabetic retinopathy. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4598. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Oxidative stress plays an important role in the development of diabetic retinopathy, and administration of antioxidants (including vitamins and lipoic acid) to diabetic rats prevents its development. Carotenoids are nutritionally important and are considered as powerful antioxidants. Among these carotenoids, lutein and zeaxanthin (Zx) are specifically concentrated in the macula. Diabetes has been shown to decrease the levels of leutin and Zx in the serum, and Zx in the retina. Our aim is to investigate the effect of carotenoid-rich antioxidants (C-AO) on the development of diabetic retinopathy.
A group of rats, soon after induction of diabetes by streptozotocin, were fed for ~11 months Purina 5001 diet supplemented with C-AO including Zx, lutein, lipoic acid and omega-3 fatty acids. The other group of diabetic rats received Purina 5001 without any supplementation. Retinal function was evaluated at ~ 4 months of diabetes by quantifying rod-mediated b-wave amplitude. After ~11 months of diabetes, retinal vasculature was prepared by trypsin-digestion to measure capillary cell apoptosis (TUNEL-staining) and histopathology (degenerative capillaries). The retina from the other eye was used to measure mitochondrial damage by quantifying the gene expressions of mtDNA-encoded proteins of complex I (ND1) and complex III (cytochrome b).
At ~4 months of diabetes, the amplitude of b-wave was significantly lower compared to age-matched normal rats. At ~11 months of diabetes, retinal vasculature of the same animals had higher number (3-4 fold) of TUNEL-positive cells and degenerative capillaries. Mitochondria were damaged as evidenced by decreased gene expressions of ND1 and cytochrome b. Supplementation with C-AO ameliorated diabetes-induced alterations in retinal function, capillary cell apoptosis and the development of diabetic retinopathy; b-wave amplitude was higher, the number of degenerative capillaries and TUNEL-positive cells were significantly lower, and mtDNA-encoded genes were higher in C-AO rats compared to non-treated diabetic rats.
Carotenoids have potential to prevent retinal dysfunction and the development of diabetic retinopathy, and the mechanism appears to be via protecting mitochondria integrity. Thus, supplementation with carotenoids could represent an achievable and inexpensive adjunct therapy to inhibit the development of diabetic retinopathy.
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