. Association of Antioxidant Markers (SOD, GSH, NO, Catalase) with Ischemic Stroke Severity and Recovery Outcomes
Markers (SOD, GSH, NO, Catalase) with Ischemic Stroke Severity
Abstract
Objective: The aim of this study was to investigate the relationship between antioxidant markers (Superoxide Dismutase [SOD], Glutathione [GSH], Catalase, and Nitric Oxide [NO]) and the severity of ischemic stroke in affected individuals.
Methods: A randomized controlled, single-blind study was conducted from June 2022 to November 2024. The study included 364 patients aged 45-80 years diagnosed with ischemic stroke. Participants were randomly divided into two groups: Group A (n=193) received standard stroke rehabilitation therapy, while Group B (n=171) received additional antioxidant support. Serum levels of SOD, GSH, Catalase, and NO were measured. The severity of ischemic stroke was evaluated using the modified Rankin Scale (mRS) and NIH Stroke Scale (NIHSS), with follow-up evaluations conducted at 2-, 4-, and 6-months post-treatment.
Results: Among the 364 participants, 203 (55.7%) were male, and 161 (44.3%) were female, with a mean age of 67.3 ± 12.2 years. Serum SOD levels were higher in the experimental group (16.3 ± 3.7 U/mL) compared to the control group (12.5 ± 4.1 U/mL, p = 0.014). GSH levels were also significantly higher in the experimental group (178 ± 31 μmol/L) than in the control group (145 ± 26 μmol/L, p = 0.032). NO levels were higher in the experimental group (42.1 ± 8.6 μmol/L) than in the control group (35.4 ± 7.3 μmol/L, p = 0.021). Catalase levels were 52.3 ± 11.1 U/mL in the experimental group and 49.6 ± 10.2 U/mL in the control group, with no significant difference between the groups (p = 0.213). Significant inverse correlations were found between SOD, GSH, and NO levels and stroke severity (p < 0.05), but catalase showed no such correlation (p = 0.513).
Conclusion: This study identified a significant relationship between lower levels of SOD, GSH, and NO and more severe ischemic stroke outcomes. Higher levels of these antioxidants were associated with improved recovery. In contrast, catalase did not show a significant association with stroke severity or recovery, suggesting that SOD, GSH, and NO may play a more critical role in the pathophysiology of ischemic stroke.
References
2. Kuriakose D, Xiao Z. Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives. Int J Mol Sci. 2020;21(20).
3. Salaudeen MA, Bello N, Danraka RN, Ammani ML. Understanding the Pathophysiology of Ischemic Stroke: The Basis of Current Therapies and Opportunity for New Ones. Biomolecules. 2024;14(3).
4. Boehme AK, Esenwa C, Elkind MS. Stroke Risk Factors, Genetics, and Prevention. Circ Res. 2017;120(3):472-95.
5. Rodrigo R, Fernández-Gajardo R, Gutiérrez R, Matamala JM, Carrasco R, Miranda-Merchak A, et al. Oxidative stress and pathophysiology of ischemic stroke: novel therapeutic opportunities. CNS Neurol Disord Drug Targets. 2013;12(5):698-714.
6. Pizzino G, Irrera N, Cucinotta M, Pallio G, Mannino F, Arcoraci V, et al. Oxidative Stress: Harms and Benefits for Human Health. Oxid Med Cell Longev. 2017;2017:8416763.
7. Garbarino VR, Orr ME, Rodriguez KA, Buffenstein R. Mechanisms of oxidative stress resistance in the brain: Lessons learned from hypoxia tolerant extremophilic vertebrates. Arch Biochem Biophys. 2015;576:8-16.
8. Lee KH, Cha M, Lee BH. Neuroprotective Effect of Antioxidants in the Brain. Int J Mol Sci. 2020;21(19).
9. Phaniendra A, Jestadi DB, Periyasamy L. Free radicals: properties, sources, targets, and their implication in various diseases. Indian J Clin Biochem. 2015;30(1):11-26.
10. Chaudhary P, Janmeda P, Docea AO, Yeskaliyeva B, Abdull Razis AF, Modu B, et al. Oxidative stress, free radicals and antioxidants: potential crosstalk in the pathophysiology of human diseases. Front Chem. 2023;11:1158198.
11. Weydert CJ, Cullen JJ. Measurement of superoxide dismutase, catalase and glutathione peroxidase in cultured cells and tissue. Nat Protoc. 2010;5(1):51-66.
12. Kozlov AV, Javadov S, Sommer N. Cellular ROS and Antioxidants: Physiological and Pathological Role. Antioxidants (Basel). 2024;13(5).
13. Nandi A, Yan LJ, Jana CK, Das N. Role of Catalase in Oxidative Stress- and Age-Associated Degenerative Diseases. Oxid Med Cell Longev. 2019;2019:9613090.
14. Abdelsalam SA, Renu K, Zahra HA, Abdallah BM, Ali EM, Veeraraghavan VP, et al. Polyphenols Mediate Neuroprotection in Cerebral Ischemic Stroke-An Update. Nutrients. 2023;15(5).
15. Kamal FZ, Lefter R, Jaber H, Balmus IM, Ciobica A, Iordache AC. The Role of Potential Oxidative Biomarkers in the Prognosis of Acute Ischemic Stroke and the Exploration of Antioxidants as Possible Preventive and Treatment Options. Int J Mol Sci. 2023;24(7).
16. Zhang HQ, Shi J, Yue T, Weng JH, Wang XL, Wang H, et al. Association between composite dietary antioxidant index and stroke among individuals with diabetes. World J Diabetes. 2024;15(8):1742-52.
17. Shirley R, Ord EN, Work LM. Oxidative Stress and the Use of Antioxidants in Stroke. Antioxidants (Basel). 2014;3(3):472-501.
18. Chen R, Liu H, Zhang G, Zhang Q, Hua W, Zhang L, et al. Antioxidants and the risk of stroke: results from NHANES and two-sample Mendelian randomization study. Eur J Med Res. 2024;29(1):50.
19. Allen CL, Bayraktutan U. Oxidative stress and its role in the pathogenesis of ischaemic stroke. Int J Stroke. 2009;4(6):461-70.
20. Jomova K, Raptova R, Alomar SY, Alwasel SH, Nepovimova E, Kuca K, et al. Reactive oxygen species, toxicity, oxidative stress, and antioxidants: chronic diseases and aging. Arch Toxicol. 2023;97(10):2499-574.
21. Chidambaram SB, Anand N, Varma SR, Ramamurthy S, Vichitra C, Sharma A, et al. Superoxide dismutase and neurological disorders. IBRO Neurosci Rep. 2024;16:373-94.
22. Younus H. Therapeutic potentials of superoxide dismutase. Int J Health Sci (Qassim). 2018;12(3):88-93.
23. Zhang MS, Liang JH, Yang MJ, Ren YR, Cheng DH, Wu QH, et al. Low Serum Superoxide Dismutase Is Associated With a High Risk of Cognitive Impairment After Mild Acute Ischemic Stroke. Front Aging Neurosci. 2022;14:834114.
24. Maksimova MY, Ivanov AV, Virus ED, Nikiforova KA, Ochtova FR, Suanova ET, et al. Impact of glutathione on acute ischemic stroke severity and outcome: possible role of aminothiols redox status. Redox Rep. 2021;26(1):117-23.
25. Wang H, Du YS, Xu WS, Li CJ, Sun H, Hu KR, et al. Exogenous glutathione exerts a therapeutic effect in ischemic stroke rats by interacting with intrastriatal dopamine. Acta Pharmacol Sin. 2022;43(3):541-51.
26. Ivanov AV, Maksimova MY, Nikiforova KA, Ochtova FR, Suanova ET, Alexandrin VVe, et al. Plasma glutathione as a risk marker for the severity and functional outcome of acute atherothrombotic and cardioembolic stroke. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery. 2022;58(1):15.
27. Jiang X, Andjelkovic AV, Zhu L, Yang T, Bennett MVL, Chen J, et al. Blood-brain barrier dysfunction and recovery after ischemic stroke. Prog Neurobiol. 2018;163-164:144-71.
28. Winovich DT, Longstreth WT, Jr., Arnold AM, Varadhan R, Zeki Al Hazzouri A, Cushman M, et al. Factors Associated With Ischemic Stroke Survival and Recovery in Older Adults. Stroke. 2017;48(7):1818-26.
29. Žitňanová I, Šiarnik P, Kollár B, Chomová M, Pazderová P, Andrezálová L, et al. Oxidative Stress Markers and Their Dynamic Changes in Patients after Acute Ischemic Stroke. Oxid Med Cell Longev. 2016;2016:9761697.
30. Pinoșanu EA, Surugiu R, Burada E, Pîrșcoveanu D, Stănciulescu CE, Sandu RE, et al. Oxidative Stress and Antioxidant Defense Mechanisms in Acute Ischemic Stroke Patients with Concurrent COVID-19 Infection. Int J Mol Sci. 2023;24(23).
Copyright (c) 2025 Wu Shengxian

This work is licensed under a Creative Commons Attribution 4.0 International License.
The published articles will be distributed under the Creative Commons Attribution 4.0 International License (CC BY). It is allowed to copy and redistribute the material in any medium or format, and remix, transform, and build upon it for any purpose, even commercially, as long as appropriate credit is given to the original author(s), a link to the license is provided and it is indicated if changes were made. Users are required to provide full bibliographic description of the original publication (authors, article title, journal title, volume, issue, pages), as well as its DOI code. In electronic publishing, users are also required to link the content with both the original article published in Journal of Medical Biochemistry and the licence used.
Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
