Lipid Peroxidation and Detection of Pro-Inflammatory Variables in Rheumatoid Arthritis- A Comprehensive Analysis of Malondialdehyde and Isoprostanes in Synovial Fluids and SERA
Assessing Lipid Peroxidation and Inflammation in Rheumatoid Arthritis
DOI:
https://doi.org/10.69750/dmls.01.02.019Keywords:
Rheumatoid Arthritis, oxidative stress, lipid peroxidation, malondialdehyde, isoprostanes.Abstract
Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease marked by systemic inflammation and joint destruction produced mostly by oxidative stress and lipid peroxidation. Analyzing markers for these processes is critical to understanding the etiology of RA.
Objectives: The goal of this study is to assess the importance of the lipid peroxidation indicators malondialdehyde (MDA) and isoprostanes in RA synovial fluids and sera in indicating oxidative stress, as well as their potential diagnostic use.
Methodology: We carried up cross-sectional analytical study with 60 participants, evenly divided between RA patients and healthy controls of the same age and gender. Malondialdehyde levels were measured spectrophotometrically using the thiobarbituric acid reactive substances (TBARS) method, and isoprostanes were quantified using commercially available ELISA kits. The samples were obtained at the Arif Clinical and Diagnostic Centre and examined in the biochemical labs of Rashid Latif Hospital in Lahore.
Results: The study found that RA patients had significantly higher levels of MDA and isoprostanes in their serum (MDA: 1.95±0.094 µmol/ml; Isoprostanes: 12.26±5.26 pg/ml) and synovial fluid (MDA: 3.26±0.65 µmol/ml; Isoprostanes: 34.26±4.26 pg/ml) compared to controls (MDA: 0.95±0.019 µmol/ml; Synovial Fluid MDA: 0.019±0.0016).
Conclusion: Elevated levels of MDA and isoprostanes in RA patients highlight their significance as oxidative stress indicators, representing the continuous inflammatory process and probable joint damage in RA. These findings lend credence to the diagnostic and prognostic value of lipid peroxidation products in the treatment of RA.
Downloads
References
Alturfan AA, Uslu E, Alturfan EE, Hatemi G, Fresko I, Kokoglu K. Increased serum sialic acid levels in primary osteoarthritis and inactive rheumatoid arthritis. Tohoku J Exp Med., 2007; 213: 241-48.
Bae SC, Kim SJ, Sung MK. Inadequate antioxidant nutrient intake and altered plasma antioxidant status of rheumatoid arthritis patients. J Am Coll Nutr., 2003; 22: 311-15.
Barrouin-Melo SM, Anturaniemi J, Sankari S, Griinari M, Atroshi F, Ounjaijean S, Hielm-Björkman AK. Evaluating oxidative stress, serological-and haematologica l status of dogs suffering from osteoarthritis, after supplementing their diet with fish or corn oil. Lipids in health and disease. 2016 Dec;15:1-7.
Baskol G, Demir H, Baskol M. Investigation of protein oxidation and lipid peroxidation in patients with rheumatoid arthritis. Cell Biochemistry and Function, 2006; 24(4): 307-11.
Blair IA. DNA adducts with lipid peroxidation products. The Journal of Biological Chemistry, 2008; 15545-49.
Catala A. Five decades with polyunsaturated fatty acids: chemical synthesis, enzymatic formation, lipid peroxidation and its biological effects. J Lipids, 2013; 2013: 19.
Cojocaru M, Cojocaru IM, Silosi I, Vrabie CD, Tanasescu R. Extra-articular Manifestations in Rheumatoid Arthritis. Mædica, 2010; 5(4): 286-91.
Crowson CS, Matteson EL, Davis JM, Gabriel SE. Contribution of Obesity to the Rise in Incidence of Rheumatoid Arthritis. Arthritis care & research, 2013; 65(1): 71-77.
Fonseca LJ, Nunes-Souza V, Goulart MO, Rabelo LA. Oxidative stress in rheumatoid arthritis: What the future might hold regarding novel biomarkers and add-on therapies. Oxidative medicine and cellular longevity. 2019 Oct;2019.
Fonseca LJ, Nunes-Souza V, Goulart MO, Rabelo LA. Oxidative stress in rheumatoid arthritis: What the future might hold regarding novel biomarkers and add-on therapies. Oxidative medicine and cellular longevity. 2019 Oct;2019.
Henrotin Y, Mobasheri A. Soluble Proteomic Biomakers in the Management of Arthritis. InStudies on Arthritis and Joint Disorders 2012 Dec 24 (pp. 3-31). New York, NY: Springer New York.
Hughes D. Measurement and evaluation of biomarkers of oxidative stress, inflammation, haemorheology and whole blood antioxidant capacity in healthy, rheumatoid arthritis and Parkinson’s disease populations. 2018.
Ismail MM, Alaaraji SF. An exploration of the relationship between interleukin 37, 8-ohdg and a number of anthropometric measurements in iraqi rheumatoid arthritis patients. EurAsian Journal of BioSciences. 2020 Jan 1;14(1).
Lakshmi S. Estimation of Lipid Peroxidation Levels and Superoxide Dismutase Activity in Gingival Tissue Extracts of Chronic Periodontitis-A Clinico Biochemical Study (Doctoral dissertation, Rajiv Gandhi University of Health Sciences (India)).
Łuczaj W, Gindzienska-Sieskiewicz E, Jarocka-Karpowicz I, Andrisic L, Sierakowski S, Zarkovic N, Waeg G, Skrzydlewska E. The onset of lipid peroxidation in rheumatoid arthritis: consequences and monitoring. Free radical research. 2016 Mar 3;50(3):304-13.
Marie D, Ateba G, Felicite KD, Fernando KL, Chia M, Henry LN. Oxidative Stress in Patients with Chronic Inflammatory Diseases in a Tertiary Health Care Setting in Africa. J. Autoimmun. Disord. 2017;3:47.
Martu MA, Surlin P, Lazar L, Maftei GA, Luchian I, Gheorghe DN, Rezus E, Toma V, Foia LG. Evaluation of oxidative stress before and after using laser and photoactivation therapy as adjuvant of non-surgical periodontal treatment in patients with rheumatoid arthritis. Antioxidants. 2021 Feb 3;10(2):226.
Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. J Anal Biochem, 1979; 95: 351-58.
Phillips DC, Dias HI, Kitas GD, Griffiths HR. Aberrant reactive oxygen and nitrogen species generation in rheumatoid arthritis (RA): causes and consequences for immune function, cell survival, and therapeutic intervention. Antioxidants & redox signaling. 2010 Mar 15;12(6):743-85.
Quiñonez-Flores CM, González-Chávez SA, Del Río Nájera D, Pacheco-Tena C. Oxidative Stress Relevance in the Pathogenesis of the Rheumatoid Arthritis: A Systematic Review. Bio Med Research International, 2016; 2016; 6097417.
Rajendran P, Nandakumar N, Rengarajan T, Palaniswami R, Gnanadhas EN, Lakshminarasaiah U, Gopas J, Nishigaki I. Antioxidants and human diseases. Clinica chimica acta. 2014 Sep 25;436:332-47.
Seven A, uzel SG, Aslan M, and Hamuryudan V. Lipid, protein, DNA oxidation and antioxidant status in rheumatoid arthritis. Clinical Biochemistry, 2008; 41: 538-43.
Tetik S, Ahmed S, Alturfan AA, Fresko I, Murat D, Sahin Y et al. Determination of oxidative stress in plasma of rheumatoid arthritis and primary osteoarthritis patients. Indian journal of biochemistry & biophysics, 2010; 353-358.
Uchida K. 4-Hydroxy-2-nonenal: a product and mediator of oxidative stress. Prog Lipid Res., 2003; 42: 318-43.
Veryard L, Jones E, Weaving G, Smith E, Cheek L, Wickramasinghe A, Tabet N. Pro-inflammatory cytokines IL-1β and TNF-α are not associated with plasma homocysteine concentration in Alzheimer's disease. Current Alzheimer Research. 2013 Feb 1;10(2):174-9.
Vyletelová V, Nováková M, Pašková Ľ. Alterations of HDL’s to piHDL’s proteome in patients with chronic inflammatory diseases, and HDL-targeted therapies. Pharmaceuticals. 2022 Oct 18;15(10):1278.
Published
Issue
Section
License
Copyright (c) 2024 DEVELOPMENTAL MEDICO-LIFE-SCIENCES
This work is licensed under a Creative Commons Attribution 4.0 International License.
The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/public domain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.