CORRELATION BETWEEN OCT MEASUREMENTS AND OXIDATIVE STRESS BIOMARKERS IN PATIENTS WITH AGE-RELATED MACULAR DEGENERATION

Authors

  • Raluca Eugenia IORGA “Grigore T. Popa” University of Medicine and Pharmacy Iasi
  • Andreea Dana MORARU “Grigore T. Popa” University of Medicine and Pharmacy Iasi
  • D. COSTIN “Grigore T. Popa” University of Medicine and Pharmacy Iasi
  • Razvana Sorina MUNTEANU-DANULESCU “Louis Pasteur” Clinical Hospital, Le Coudray, France
  • C. DANIELESCU “Grigore T. Popa” University of Medicine and Pharmacy Iasi

Abstract

Age-related macular degeneration (AMD) is a neurodegenerative disease that affects the central retina and is the most frequent cause of irreversible blindness in the elderly population. Aim: to establish correlations between functional and structural changes and oxidative stress markers before and after treatment in patients diagnosed with AMD. We wanted to estimate the association of the oxidative stress with the occurrence of age-related macular degeneration. Materials and methods: This are a case-control study that included a group of 59 patients diagnosed with age related macular degeneration (23 dry AMD and 36 exudative AMD), and a control group that included 62 patients. They were followed over a period of 12 months by assessment of optical coherence tomography measurements and oxidative stress markers. The oxidative stress markers included superoxide-dismutase (SOD) and thiobarbituric acid reactive substances (TBARS). Results: The mean values of SOD and TBARS were significantly higher in the study group compared to the control group. We observed higher values in patients with exudative form of AMD. Even after treatment, the mean values remained higher than in controls. The standard linear regression analysis of the mean retinal thickness values for each individual test, confirmed that the connection between SOD, TBARS and mean retinal thickness meets the requirements of a valid linear regression and SOD and TBARS can be considered to be predictors. Conclusions: Increased oxidative stress, which causes oxidative damage to lipids and proteins, may lead to irreversible damage in AMD. Investigating the neuroprotection provided by antioxidants against AMD may be helpful to further entrench the significant role of oxidative stress in AMD.

Author Biographies

  • Raluca Eugenia IORGA, “Grigore T. Popa” University of Medicine and Pharmacy Iasi

    Faculty of Medicine
    Department of Surgery (II)
    “Prof. Dr. N. Oblu” Emergency Clinical Hospital, Iași, Romania

  • Andreea Dana MORARU, “Grigore T. Popa” University of Medicine and Pharmacy Iasi

    Faculty of Medicine
    Department of Surgery (II)
    “Prof. Dr. N. Oblu” Emergency Clinical Hospital, Iași, Romania

  • D. COSTIN, “Grigore T. Popa” University of Medicine and Pharmacy Iasi

    Faculty of Medicine
    Department of Surgery (II)
    “Prof. Dr. N. Oblu” Emergency Clinical Hospital, Iași, Romania

  • C. DANIELESCU, “Grigore T. Popa” University of Medicine and Pharmacy Iasi

    Faculty of Medicine
    Department of Surgery (II)
    “Prof. Dr. N. Oblu” Emergency Clinical Hospital, Iași, Romania

References

1. Adelson JD, Bourne RRA. Causes of blindness and vision impairment in 2020 and trends over 30 years, and prevalence of avoidable blindness in relation to vision 2020: The right to sight: An analysis for the global burden of disease study. Lancet Glob Health 2021; 9: e144-e160.
2. Jonas JB, Cheung CMG. Updates on the epidemiology of age-related macular degeneration. Asia Pac J Ophthalmol 2017; 6: 493-497.
3. De Jong PTVM. A historical analysis of the quest for the origins of aging macula disorder, the tissues involved, and its terminology: Supplementary issue: Ophthalmic history. Ophthalmol Eye Dis 2016; 8: 5-14.
4. Datta S, Cano M, Ebrahimi K, Wang L, Handa JT. The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD. Prog Retin Eye Res 2017, 60: 201-218.
5. Jarrett SG, Boulton ME. Consequences of oxidative stress in age-related macular degeneration. Mo-lecular Aspects of Medicine 2012; 33(4): 399-417.
6. Coleman HR, Chan CC, Ferris FL, Chew EY. Age-related macular degeneration. Lancet 2008, 372: 1835-1845.
7. Hyttinen JMT, Błasiak J, Niittykoski M. DNA damage response and autophagy in the degeneration of retinal pigment epithelial cells-Implications for age-related macular degeneration (AMD) Ageing Res Rev 2017; 36: 64-77.
8. Yeo NJY, Chan EJJ. Choroidal neovascularization: Mechanisms of endothelial dysfunction. Front. Pharmacol 2019; 10: 1363.
9. Ruan Y, Jiang S, Gericke A. Age-Related Macular Degeneration: Role of Oxidative Stress and Blood Vessels. Int J Mol Sci 2021; 22: 1296.
10. Golestaneh N, Chu Y, Cheng SK, et al. Repressed SIRT1/PGC-1a pathway and mitochondrial disin-tegration in iPSC-derived RPE disease model of age-related macular degeneration. J Transl Med 2016; 14: 344.
11. Blasiak J, Petrovski G, Veréb Z, Facskó A, Kaarniranta K. Oxidative stress, hypoxia, and autophagy in the neovascular processes of age-related macular degeneration. Biomed Res Int 2014; 2014: 768026.
12. Totan Y, Yağcı R, Bardak Y. Oxidative macromolecular damage in age-related macular degeneration. Current Eye Research 2009; 34(12): 1089-1093.
13. Evereklioglu C, Er H, Doganay S, et al. Nitric oxide and lipid peroxidation are increased and associated with decreased antioxidant enzyme activities in patients with age-related macular degeneration. Doc Ophthalmol 2003; 106: 129-136.
14. Yildirim Z, Ucgun NI, Yildirim F. The role of oxidative stress and antioxidants in the pathogenesis of age-related macular degeneration. Clinics 2011; 66(5): 743-746.
15. Jia L, Dong Y, Yang H, et al. Serum superoxide dismutase and malondialdehyde levels in a group of Chinese patients with age-related macular degeneration. Aging Clin Exp Res 2011; 23(4): 264-267.
16. Matsuura T, Takayama K, Kaneko H, et al. Nutritional Supplementation Inhibits the Increase in Serum Malondialdehyde in Patients with Wet Age-Related Macular Degeneration. Oxid Med Cell Longev 2017; 2017: 9548767.
17. Dong A, Xie B, Shen J, et al. Oxidative stress promotes ocular neovascularization. J. Cell Physiol 2009; 219: 544-552.
18. Ye F, Kaneko H, Hayashi Y, Takayama K, Hwang SJ. Malondialdehyde induces autophagy dysfunc-tion and VEGF secretion in the retinal pigment epithelium in age-related macular degeneration. Free Radic Biol Med 2016; 94: 121-134.
19. Kim SY, Kambhampati SP, Bhutto IA, McLeod DS, Lutty GA, Kannan RM. Evolution of oxidative stress, inflammation and neovascularization in the choroid and retina in a subretinal lipid induced age-related macular degeneration model. Exp Eye Res 2021; 203: 108391.
20. Hollyfield JG, Crabb JW, Salomon RG. Proteomic approaches to understanding age-related macular degeneration. Adv Exp Med Biol 2003; 533: 83-89.
21. Teper SJ, Nowińska A, Figurska M, Rękas M, Wylęgała E. The Need for Treatment of Neovascular Age-Related Macular Degeneration: A Study Based on the Polish National Registry. Ophthalmol Ther 2022; 11(5): 1805-1816.
22. De Cillà S, Farruggio S, Vujosevic S, et al. Anti-Vascular Endothelial Growth Factors Protect Retinal Pigment Epithelium Cells Against Oxidation by Modulating Nitric Oxide Release and Autophagy. Cell Physiol. Biochem 2017; 42: 1725-1738.
23. Sheu SJ, Chao YM, Liu NC, Chan JY. Differential effects of bevacizumab, ranibizumab and aflibercept on cell viability, phagocytosis and mitochondrial bioenergetics of retinal pigment epithelial cell. Acta Ophthalmol. 2015; 93:e631-e643.
24. De Cillà, S, Farruggio, S, Cocomazzi, G, et al. Aflibercept and Ranibizumab Modulate Retinal Pigment Epithelial Cells Function by Acting on Their Cross Talk with Vascular Endothelial Cells. Cell Physiol. Biochem 2020; 54: 161-179.

Additional Files

Published

2023-12-21