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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Cytokines and inflammation</journal-id><journal-title-group><journal-title xml:lang="en">Cytokines and inflammation</journal-title><trans-title-group xml:lang="ru"><trans-title>Цитокины и воспаление</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1684-7849</issn><publisher><publisher-name xml:lang="en">Eco-Vector</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">629601</article-id><article-id pub-id-type="doi">10.17816/CI629601</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Reviews</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Научные обзоры</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Oxidative stress as a marker of inflammation in cataracts</article-title><trans-title-group xml:lang="ru"><trans-title>Окислительный стресс как признак воспаления при катаракте</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3992-9207</contrib-id><name-alternatives><name xml:lang="en"><surname>Smirnova</surname><given-names>O. V.</given-names></name><name xml:lang="ru"><surname>Смирнова</surname><given-names>Ольга Валентиновна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>доктор медицинских наук, профессор, заведующая лабораторией клинической патофизиологии </p></bio><email>ovsmirnova71@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0003-0587-4452</contrib-id><name-alternatives><name xml:lang="en"><surname>Zinkina</surname><given-names>T. O.</given-names></name><name xml:lang="ru"><surname>Зинкина</surname><given-names>Татьяна Олеговна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>аспирант</p></bio><email>tatka-doktor@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Research Institute for Medical Problems in the North - Division of Federal Research Center «Krasnoyarsk Scientific Center of the Siberian Branch of the RAS»</institution></aff><aff><institution xml:lang="ru">ФГБНУ «Федеральный исследовательский центр «Красноярский научный центр» СО РАН обособленное подразделение «Научно-исследовательский институт медицинских проблем Севера»</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2023-12-22" publication-format="electronic"><day>22</day><month>12</month><year>2023</year></pub-date><volume>20</volume><issue>3</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>3</fpage><lpage>8</lpage><history><date date-type="received" iso-8601-date="2024-03-29"><day>29</day><month>03</month><year>2024</year></date><date date-type="accepted" iso-8601-date="2024-03-29"><day>29</day><month>03</month><year>2024</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2023, Smirnova O.V., Zinkina T.O.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2023, Смирнова О.В., Зинкина Т.О.</copyright-statement><copyright-year>2023</copyright-year><copyright-holder xml:lang="en">Smirnova O.V., Zinkina T.O.</copyright-holder><copyright-holder xml:lang="ru">Смирнова О.В., Зинкина Т.О.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/" start_date="2026-04-11"/></permissions><self-uri xlink:href="https://cijournal.ru/1684-7849/article/view/629601">https://cijournal.ru/1684-7849/article/view/629601</self-uri><abstract xml:lang="en"><p><bold>Introduction.</bold> Oxidative stress is an important pathogenetic factor of degenerative eye diseases. Oxidative stress can damage tissues, leading to changes in their structure and function, increased vascular permeability, microvascular abnormalities and neovascularization. In turn, these changes can cause damage to the eye; denaturation of the crystalline lens.</p> <p><bold>The purpose of the study:</bold> according to modern literature, to study the role of oxidative stress and inflammation in the development of cataracts.</p> <p>The molecular mechanisms of cell damage under oxidative stress and the pathogenesis of cataracts caused by oxidative stress have been studied.</p> <p><bold>Conclusion. </bold>Oxidative stress is an important pathogenetic mechanism of degenerative eye diseases. Oxidized phospholipids activate pro-inflammatory molecules and cause inflammation. Oxidative stress in the body is regulated by antioxidant mechanisms. An imbalance of antioxidants affects the lens and causes cataracts. The G/G genotype of SOD1-251 A/G polymorphism may lead to a higher risk of senile cataracts. The content of antioxidants depends on the density of the lens nuclei, on the type of cataract. Non-enzymatic antioxidants have a predominant effect in watery moisture, and enzymatic antioxidants in blood serum in patients with cataracts.</p></abstract><trans-abstract xml:lang="ru"><p><bold>Введение. </bold>Окислительный стресс является важным патогенетическим фактором дегенеративных заболеваний глаз. Он может повреждать ткани, приводя к изменениям их структуры и функции, повышению проницаемости сосудов, микрососудистым аномалиям и неоваскуляризации. В свою очередь, эти изменения могут вызывать поражение глаза, денатурацию кристаллина хрусталика.</p> <p><bold>Цель исследования </bold>–<bold> </bold>по данным современной литературы изучить роль окислительного стресса и воспаления при развитии катаракты.</p> <p>Изучены молекулярные механизмы повреждения клеток при окислительном стрессе и патогенез катаракты, обусловленный окислительным стрессом.</p> <p><bold>Вывод.</bold> Окислительный стресс является важным патогенетическим механизмом дегенеративных заболеваний глаз. Окисленные фосфолипиды активируют провоспалительные молекулы и вызывают воспаление. Окислительный стресс в организме регулируется антиоксидантными механизмами. Дисбаланс антиоксидантов поражает хрусталик и вызывает катаракту. Генотип G/G полиморфизма SOD1-251 A/G может привести к более высокому риску старческой катаракты. Содержание антиоксидантов зависит от плотности хрусталиковых ядер, от вида катаракты. Неферментативные антиоксиданты оказывают преимущественное влияние в водянистой влаге, а ферментативные антиоксиданты – в сыворотке крови у больных с катарактой.</p></trans-abstract><kwd-group xml:lang="en"><kwd>cataracts</kwd><kwd>oxidative stress</kwd><kwd>SOD1</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>катаракта</kwd><kwd>окислительный стресс</kwd><kwd>SOD1</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Nita, M.; Grzybowski, A. The role of the reactive oxygen species and oxidative stress in the pathomechanism of the age-related ocular diseases and other pathologies of the anterior and posterior eye segments in adults //Oxidative Med. Cell. Longev- 2016. -V.2016, Р. 3164734. doi: 10.1155/2016/3164734.</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Sunkireddy, P.; Jha, S.N.; Kanwar, J.R.; Yadav, S.C. Natural antioxidant biomolecules promises future nanomedicine based therapy for cataract // Colloids Surf. B Biointerfaces - 2013. - V. 112. P. 554–562. doi: 10.1016/j.colsurfb.2013.07.068.</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Sies, H.; Berndt, C.; Jones, D.P. Oxidative Stress // Annu. Rev. Biochem. - 2017. - V. 86. P. 715–748. doi: 10.1146/annurev-biochem-061516-045037.</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Bochkov, V.N.; Oskolkova, O.V.; Birukov, K.G.; Levonen, A.L.; Binder, C.J.; Stöckl, J. Generation and biological activities of oxidized phospholipids // Antioxid. Redox Signal. - 2010. - V. 12. P. 1009–1059. doi:10.1155/2019/5080843.</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Di Gioia, M.; Zanoni, I. Dooming phagocyte responses: inflammatory effects of endogenous oxidized phospholipids // Front. Endocrinol. - 2021. - V. 12. P. 626842. doi: 10.3389/fendo.2021.626842.</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Sadowska-Bartosz, I.; Bartosz, G.; Grune, T.; Sereikaite, J. Role of oxidative, nitrative, and chlorinative protein modifications in aging and age-related diseases // Oxidative Med. Cell. Longev. - 2018. - V. 2018. P. 3267898. doi: 10.1155/2018/3267898.</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Shokolenko, I.; Venediktova, N.; Bochkareva, A.; Wilson, G.L.; Alexeyev, M.F. Oxidative stress induces degradation of mitochondrial DNA // Nucleic Acids Res. - 2009. - V. 37. P. 2539–2548. doi: 10.1155/2018/3267898.</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Finkel, T. Signal transduction by reactive oxygen species // J. Cell Biol. - 2011. - V. 194. P. 7–15. doi: 10.1093/nar/gkp100.</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Evans, M.D.; Dizdaroglu, M.; Cooke, M.S. Oxidative DNA damage and disease: induction, repair and significance // Mutat. Res. - 2004. - V. 567, p. 1–61. doi: 10.1083/jcb.201102095.</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Roos, W.P.; Kaina, B. DNA damage-induced cell death by apoptosis // Trends Mol. Med. - 2006. - V. 12. P. 440–450. doi: 10.1016/j.molmed.2006.07.007.</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Krishnamoorthy, R.R.; Crawford, M.J.; Chaturvedi, M.M.; Jain, S.K.; Aggarwal, B.B.; Al-Ubaidi, M.R.; Agarwal, N. Photo-oxidative stress down-modulates the activity of nuclear factor-kappaB via involvement of caspase-1, leading to apoptosis of photoreceptor cells // J. Biol. Chem. - 1999. - V. 274. P. 3734–3743. doi: 10.1074/jbc.274.6.3734.</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Aitbaev, K.A.; Murkamilov, I.T.; Fomin, V.V. Molecular mechanisms of aging: The role of oxidative stress and epigenetic modifications // Adv. Gerontol. - 2019. - V. 32. P. 20–28. doi: 10.1134/S2079057019040027.</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Nakka, V.P.; Prakash-Babu, P.; Vemuganti, R. Crosstalk between endoplasmic reticulum stress, oxidative stress, and autophagy: potential therapeutic targets for acute CNS injuries // Mol. Neurobiol. - 2016. - V. 53. P. 532–544. doi: 10.1007/s12035-014-9029-6.</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Filomeni, G.; De Zio, D.; Cecconi, F. Oxidative stress and autophagy: The clash between damage and metabolic needs // Cell Death Differ. - 2015. - V. 22. P. 377–388. doi: 10.1038/cdd.2014.150.</mixed-citation></ref><ref id="B15"><label>15.</label><mixed-citation>Klionsky, D.J.; Abeliovich, H.; Agostinis, P.; Agrawal, D.K.; Aliev, G.; Askew, D.; Baba, M.; Baehrecke, E.H.; Bahr, B.A.; Ballabio, A.; et al. Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes //Autophagy. - 2008. - V. 4. P. 151–175. doi: 10.4161/авто.5338.</mixed-citation></ref><ref id="B16"><label>16.</label><mixed-citation>Hsueh, Y.J.; Meir, Y.J.; Yeh, L.K.; Wang, T.K.; Huang, C.C.; Lu, T.T.; Cheng, C.M.; Wu, W.C.; Chen, H.C. Topical ascorbic acid ameliorates oxidative stress-induced corneal endothelial damage via suppression of apoptosis and autophagic flux blockage // Cells. - 2020. - V. 9. P. 943. doi: 10.3390/cells9040943.</mixed-citation></ref><ref id="B17"><label>17.</label><mixed-citation>Yan, X.Y.; Zhong, X.R.; Yu, S.H.; Zhang, L.C.; Liu, Y.N.; Zhang, Y.; Sun, L.K.; Su, J. P62 aggregates mediated Caspase 8 activation is responsible for progression of ovarian cancer // J. Cell. Mol. Med. - 2019. - V. 23. P. 4030–4042. doi: 10.1111/jcmm.14288.</mixed-citation></ref><ref id="B18"><label>18.</label><mixed-citation>Laporte, C.; Kosta, A.; Klein, G.; Aubry, L.; Lam, D.; Tresse, E.; Luciani, M.F.; Golstein, P. A necrotic cell death model in a protist // Cell Death Differ. - 2007. - V.14. P. 266–274. doi: 10.1038/sj.cdd.4401994.</mixed-citation></ref><ref id="B19"><label>19.</label><mixed-citation>Ali, S.S.; Ahsan, H.; Zia, M.K.; Siddiqui, T.; Khan, F.H. Understanding oxidants and antioxidants: Classical team with new players // J. Food Biochem. - 2020. - V. 44. P. e13145. doi: 10.1111/jfbc.13145.</mixed-citation></ref><ref id="B20"><label>20.</label><mixed-citation>Kurutas, E.B. The importance of antioxidants which play the role in cellular response against oxidative nitrosative stress: Current state // Nutr. J. - 2016. - V. 15, P. 71. doi: 10.1111/jfbc.13145.</mixed-citation></ref><ref id="B21"><label>21.</label><mixed-citation>Lu, J.; Holmgren, A. The thioredoxin antioxidant system // Free Radic. Biol. Med. - 2014. - V. 66, P. 75–87. doi: 10.1016/j.freeradbiomed.2013.07.036.</mixed-citation></ref><ref id="B22"><label>22.</label><mixed-citation>Singhal, S.S.; Singh, S.P.; Singhal, P.; Horne, D.; Singhal, J.; Awasthi, S. Antioxidant role of glutathione S-transferases: 4- Hydroxynonenal, a key molecule in stress-mediated signaling //Toxicol. Appl. Pharmacol. - 2015. - V. 289, P. 361–370. doi: 10.1016/j.taap.2015.10.006.</mixed-citation></ref><ref id="B23"><label>23.</label><mixed-citation>Miron'czuk-Chodakowska, I., Witkowska, A. M., Zujko, M. E. Endogenous non-enzymatic antioxidant sinter human body // Adv. Med. Sci. - 2018. - V. 63, P. 68–78. doi: 10.1016/j.advms.2017.05.005.</mixed-citation></ref><ref id="B24"><label>24.</label><mixed-citation>Halliwell, B.; Gutteridge, J.M.C. The antioxidants of human extracellular fluids // Arch. Biochem. Biophys. - 1990 - V. 280, P. 1–8. doi: 10.1016/0003-9861(90)90510-6.</mixed-citation></ref><ref id="B25"><label>25.</label><mixed-citation>Delamere, N.A. Ascorbic acid and the eye // In Subcellular Biochemistry: Ascorbic Acid: Biochemistry and Biomedical Cell Biology/ Harris, J.R., Ed.; Springer: Boston, MA, USA. - 1996; pp. 313–329. doi: 10.1007/BF02024159.</mixed-citation></ref><ref id="B26"><label>26.</label><mixed-citation>Bragt, P.C.; Bonta, I.L. Oxidant stress during inflammation: Anti-inflammatory effects of antioxidants //Agents Actions - 1980. - V. 10. P. 536–539.</mixed-citation></ref><ref id="B27"><label>27.</label><mixed-citation>Augustin, A.J.; Dick, H.B. Oxidative tissue damage after phacoemulsification: Influence of ophthalmic viscosurgical devices // J. Cataract Refract. Surg. - 2004. - V. 30. P. 424–427. doi: 10.1016/S0886-3350(03)00577-7.</mixed-citation></ref><ref id="B28"><label>28.</label><mixed-citation>Özer, M.A.; Polat, N.; Özen, S.; Parlakpınar, H.; Ekici, K.; Polat, A.; Vardı, N.; Tanbek, K.; Yildiz, A. Effects of molsidomine on retinopathy and oxidative stress induced by radiotheraphy in rat eyes // Curr. Eye Res. - 2017. - V. 42. P. 803–809. doi: 10.1080/02713683.2016.1238943.</mixed-citation></ref><ref id="B29"><label>29.</label><mixed-citation>Bergandi, L.; Skorokhod, O.A.; Franzone, F.; La Grotta, R.; Schwarzer, E.; Nuzzi, R. Induction of oxidative stress in human aqueous and vitreous humors by Nd:YAG laser posterior capsulotomy // Int. J. Ophthalmol. - 2018. - V. 11. P. 1145–1151.</mixed-citation></ref><ref id="B30"><label>30.</label><mixed-citation>Hull, D.S.; Green, K. Oxygen free radicals and corneal endothelium // Lens Eye Toxic. Res. - 1989. - V. 6. P. 87–91.</mixed-citation></ref><ref id="B31"><label>31.</label><mixed-citation>Kowluru, R.A.; Chan, P.S. Oxidative stress and diabetic retinopathy // Exp. Diabetes Res. - 2007. - V. 2007. P. 43603. doi: 10.1155/2007/43603.</mixed-citation></ref><ref id="B32"><label>32.</label><mixed-citation>Beatty, S.; Koh, H.; Phil, M.; Henson, D.; Boulton, M. The role of oxidative stress in the pathogenesis of age-related macular degeneration // Surv. Ophthalmol. - 2000. - V. 45. P. 115–134. doi: 10.1016/S0039-6257(00)00140-5.</mixed-citation></ref><ref id="B33"><label>33.</label><mixed-citation>Williams, D.L. Oxidative stress and the eye // Vet. Clin. N. Am. Small Anim. Pract. - 2008. - V. 38. P. 179–192. doi: 10.1016/j.cvsm.2007.10.006.</mixed-citation></ref><ref id="B34"><label>34.</label><mixed-citation>Sacca, S.C.; Roszkowska, A.M.; Izzotti, A. Environmental light and endogenous antioxidants as the main determinants of non-cancer ocular diseases // Mutat. Res. 2013. - V. 752. P. 153–171. doi: 10.1016/j.mrrev.2013.01.001.</mixed-citation></ref><ref id="B35"><label>35.</label><mixed-citation>Pascolini, D.; Mariotti, S.P. Global estimates of visual impairment: 2010 // Br. J. Ophthalmol. - 2012. - V. 96. P. 614. doi: 10.1136/bjophthalmol-2011-300539.</mixed-citation></ref><ref id="B36"><label>36.</label><mixed-citation>Moreau, K.L.; King, J.A. Protein misfolding and aggregation in cataract disease and prospects for prevention //Trends Mol. Med. - 2012. - V. 18. P. 273–282. doi: 10.1016/j.molmed.2012.03.005.</mixed-citation></ref><ref id="B37"><label>37.</label><mixed-citation>Kisic, B.; Miric, D.; Zoric, L.; Ilic, A.; Dragojevic, I. Antioxidant capacity of lenses with age-related cataract //Oxidative Med. Cell. Longev. - 2012. - V. 2012. P. 467130. doi: 10.1155/2012/467130.</mixed-citation></ref><ref id="B38"><label>38.</label><mixed-citation>Spector, A. Review: Oxidative stress and disease // J. Ocul. Pharmacol. Ther. - 2000. - V. 16. P. 193–201. doi: 10.1089/jop.2000.16.193.</mixed-citation></ref><ref id="B39"><label>39.</label><mixed-citation>Kisic, B.; Miric, D.; Zoric, L.; Ilic, A. Role of lipid peroxidation in the pathogenesis of age-related cataract // In Lipid Peroxidation; IntechOpen: Rijeka, Croatia, 2012.</mixed-citation></ref><ref id="B40"><label>40.</label><mixed-citation>Miric, D.; Kisic, B.; Zoric, L.; Miric, B.; Mirkovic, M.; Mitic, R. Influence of cataract maturity on aqueous humor lipid peroxidation markers and antioxidant enzymes // Eye. - 2014. - V. P. 28, 72. doi: 10.1038/eye.2013.207.</mixed-citation></ref><ref id="B41"><label>41.</label><mixed-citation>Zhou, Y.F.; Guo, B.; Ye, M.J.; Liao, R.F.; Li, S.L. Protective effect of rutin against H2O2-induced oxidative stress and apoptosis in human lens epithelial cells // Curr. Eye Res. - 2016. V. 41. P. 933–942. doi: 10.3109/02713683.2015.1082186.</mixed-citation></ref><ref id="B42"><label>42.</label><mixed-citation>Delamere, N.A.; Tamiya, S. Expression, regulation and function of Na,K-ATPase in the lens // Prog. Retin. Eye Res. - 2004. - V. 23. P. 593–615. doi: 10.1016/j.preteyeres.2004.06.003.</mixed-citation></ref><ref id="B43"><label>43.</label><mixed-citation>Kim, J.Y.; Park, J.H.; Kang, S.S.; Hwang, S.B.; Tchah, H. Topical nerve growth factor attenuates streptozotocin-induced diabetic cataracts via polyol pathway inhibition and Na(+)/K(+)-ATPase upregulation // Exp. Eye Res. - 2021. V. 202. P. 108319. doi: 10.1016/j.exer.2020.108319.</mixed-citation></ref><ref id="B44"><label>44.</label><mixed-citation>Chen, Y.; Mehta, G.; Vasiliou, V. Antioxidant defenses in the ocular surface // Ocul. Surf. - 2009. - V. 7. P. 176–185. doi: 10.1016/S1542-0124(12)70185-4.</mixed-citation></ref><ref id="B45"><label>45.</label><mixed-citation>Katta, A.V.; Katkam, R.V.; Geetha, H. Lipid peroxidation and the total antioxidant status in the pathogenesis of age related and diabetic cataracts: A study on the lens and blood // J. Clin. Diagn. Res. - 2013. - V. 7. P. 978–981. doi: 10.7860/JCDR/2013/4937.3099.</mixed-citation></ref><ref id="B46"><label>46.</label><mixed-citation>Babizhayev, M.A. Mitochondria induce oxidative stress, generation of reactive oxygen species and redox state unbalance of the eye lens leading to human cataract formation: Disruption of redox lens organization by phospholipid hydroperoxides as a common basis for cataract disease // Cell Biochem. Funct. - 2011. - V. 29. P. 183–206.</mixed-citation></ref><ref id="B47"><label>47.</label><mixed-citation>Zhang, Y.; Zhang, L.; Sun, D.; Li, Z.; Wang, L.; Liu, P. Genetic polymorphisms of superoxideedismutases, catalase, and glutathione peroxidase in age-related cataract // Mol. Vis. - 2011. - V. 17. P. 2325–2332.</mixed-citation></ref><ref id="B48"><label>48.</label><mixed-citation>Wang, X.; Sun, J.; Dang, G.F.; Gao, Y.; Duan, L.; Wu, X. Y. Antioxidant content and cytological examination of aqueous fluid from patients with age-related cataracts at different stages // Genet. Mol. Res. - 2015. - V. 14. P. 6251–6255. doi: 10.4238/2015.June.9.11.</mixed-citation></ref><ref id="B49"><label>49.</label><mixed-citation>Elmazar, H.M.; Elmadbouh, I.; Mandour, S.S.; Al Ariny, G.M.; Ibrahim, A.M. Association between cataract progression and ischemia-modified albumin in relation to oxidant-antioxidant profiles in the serum, aqueous humor, and lens // J. Cataract Refract. Surg. - 2018. - V. 44. P. 134–139. doi: 10.1016/j.jcrs.2017.10.051.</mixed-citation></ref><ref id="B50"><label>50.</label><mixed-citation>Yanshole, V.V.; Yanshole, L.V.; Snytnikova, O.A.; Tsentalovich, Y.P. Quantitativemetabolomic analysis of changes in the lens and aqueous humor under development of age-related nuclear cataract // Metabolomics - 2019. - V. 15. P. 29. doi: 10.1007/s11306-019-1495-4.</mixed-citation></ref><ref id="B51"><label>51.</label><mixed-citation>Krepler, K.; Schmid, R. Alpha-tocopherolinplasma, red blood cells and lenses with and without cataract // Am. J. Ophthalmol. - 2005. - V. 139. P. 266–270. doi: 10.1016/j.ajo.2004.09.031.</mixed-citation></ref><ref id="B52"><label>52.</label><mixed-citation>Zoric', L.; Aleksic', P.; Korac'evic', D.; Trajkovic', G. The aqueous humour antioxidative capacity indifferent types and color of the age-related cataract // Vojn. Pregl. - 2005. - V. 62. P. 909–913. doi: 10.2298/VSP0512909Z.</mixed-citation></ref><ref id="B53"><label>53.</label><mixed-citation>Qin, Y.J.; Chan, S.O.; Lin, H.L.; Zhang, Y.Q.; Chen, Y.L.; Niu, Y..; Xie, W.J.; Chu, W.K.; Pang, C.P.; Zhang, H.Y. Elevatedlevelof uric acid in aqueous humour is associated with posterior subcapsular cataract in human lens // Clin. Exp. Ophthalmol. - 2020. - V. 48. P. 1183–1191. doi: 10.1111/ceo.13835.</mixed-citation></ref><ref id="B54"><label>54.</label><mixed-citation>Canadananovic', V.; Latinovic', S.; Barišic', S.; Babic', N.; Jovanovic', S. Age-related changes of vitamin C levels in aqueous humour // Vojn. Pregl. - 2015. - V. 72. P. 823–826. doi: 10.2298/VSP131212063C.</mixed-citation></ref><ref id="B55"><label>55.</label><mixed-citation>Selvi, R.; Angayarkanni, N.; Biswas, J.; Ramakrishnan, S. Total antioxidant capacity in Eales’disease, uveitis&amp;cataract //Indian J. Med. Res. - 2011. - V. 134. P. 83–90.</mixed-citation></ref><ref id="B56"><label>56.</label><mixed-citation>Wang, A.; Han, J.; Jiang, Y.; Zhang, D. Association of vitamin A and β-carotenewith risk forage-related cataract: Ameta-analysis // Nutrition. - 2014. - V. 30. P. 1113–1121. doi: 10.1016/j.nut.2014.02.025.</mixed-citation></ref><ref id="B57"><label>57.</label><mixed-citation>Tsao, Y.T.; Wu, W.C.; Chen, K.J.; Yeh, L.K.; Hwang, Y.S.; Hsueh, Y.J.; Chen, H.C.; Cheng, C.M. Analysis of aqueous humor total antioxidant capacity and its correlation with corneal endothelial health // Bioeng. Transl. Med. - 2021. - V. 6. P. e10199. doi: 10.1002/btm2.10199.</mixed-citation></ref><ref id="B58"><label>58.</label><mixed-citation>Haung, W.; Koralewska-Makár, A.; Bauer, B.; Akesson, B. Extracellul arglutathioneperoxidase and ascorbicacidinaqueous humor and serum of patients operated on for cataract // Clin. Chim. Acta. - 1997. - V. 261. P. 117–130. doi: 10.1016/S0009-8981(97)06520-0.</mixed-citation></ref></ref-list></back></article>
