Journals

Journals By Subject

Life Sciences, Agriculture & Food
Chemistry
Medicine & Health
Materials Science
Mathematics & Physics
Electrical & Computer Science
Earth, Energy & Environment
Architecture & Civil Engineering
Education
Economics & Management
Humanities & Social Sciences
Multidisciplinary

Special Issues

Propose a Special Issue
Special Issue Guidelines
Ongoing Special Issues
Published Special Issues

Join Us

Become the Founding Editor-in-Chief
Join as Editor-in-Chief
Join as Senior Editor
Join as Editorial Board Member
Become a Reviewer
Submit an Article
Research Article | | Peer-Reviewed

Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue

Baykulov Azim Kenjayevich*
Published in International Journal of Cardiovascular and Thoracic Surgery (Volume 12, Issue 1)
Received: 22 September 2025     Accepted: 4 October 2025     Published: 2 February 2026
Views:       Downloads:
Download PDF
Abstract

Introduction: Myocardial infarction (MI) remains one of the most common and life-threatening cardiovascular diseases worldwide. Experimental models of MI are essential for understanding its pathophysiology and evaluating therapeutic interventions. Objective: The aim of this study was to evaluate lipid peroxidation and antioxidant defense during experimental MI in rats. Methods: MI was induced in adult male rats by ligation of the left coronary artery. On the third day after MI, cardiac and liver tissues were collected. Heart and liver homogenates, as well as mitochondrial (MF) and microsomal (MSF) fractions of the liver, were analyzed for malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity. Results: Compared with the control group, MDA concentration increased fivefold in cardiac homogenates and 6.1-fold in liver MF, while MSF showed the most pronounced increase (28.2-fold). SOD activity was significantly reduced: by 31.5% in MF and by 73.1% in MF. Conclusion: Experimental MI induces pronounced oxidative stress, characterized by excessive lipid peroxidation and suppression of antioxidant defenses. This model represents a valuable tool for investigating cardioprotective strategies and antioxidant therapy.

Published in International Journal of Cardiovascular and Thoracic Surgery (Volume 12, Issue 1)
DOI 10.11648/j.ijcts.20261201.13
Page(s) 14-17
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2026. Published by Science Publishing Group
Previous article
Keywords

Myocardial Infarction, Oxidative Stress, Lipid Peroxidation, Malondialdehyde, Superoxide Dismutase, Experimental Model

1. Introduction
Cardiovascular diseases remain the leading cause of death worldwide, accounting for over 17 million deaths annually and representing a substantial global health and economic burden. Among them, myocardial infarction (MI) remains one of the most acute and life-threatening conditions, characterized by irreversible ischemic necrosis of cardiac tissue, which often leads to heart failure, severe disability, or death. Despite significant progress in interventional cardiology and pharmacotherapy, the morbidity and mortality associated with MI remain unacceptably high. This underscores the urgent need for a deeper understanding of the molecular and biochemical processes that drive myocardial damage, which could lead to the development of novel cardioprotective strategies
[1-6]
.
Recent advances in experimental modeling provide researchers with robust and reproducible tools to mimic MI in laboratory animals, enabling the investigation of pathophysiological mechanisms under controlled conditions and facilitating preclinical testing of therapeutic agents
[7-10]
.
A key event in the pathogenesis of MI is oxidative stress, driven by excessive production of reactive oxygen species (ROS), which plays a central role in myocardial injury. Free radical lipid peroxidation (LPO) leads to structural disintegration of cellular and subcellular membranes, disrupts ion homeostasis, alters enzyme activity, and ultimately triggers cardiomyocyte death through necrotic and apoptotic pathways. The quantification of lipid peroxidation products, particularly malondialdehyde (MDA), provides a reliable biomarker of oxidative damage and allows for the assessment of oxidative stress severity
[11-15]
.
Given the close interplay between oxidative damage and antioxidant defense systems, evaluating the balance between pro-oxidant and antioxidant mechanisms is essential for identifying critical windows of therapeutic intervention
[16-18]
.
Therefore, the aim of this study was to investigate lipid peroxidation levels and antioxidant system activity in both cardiac and hepatic tissues during the early phase of experimental MI, with the goal of identifying biochemical targets for future cardioprotective therapies.
2. Materials and Methods
Twenty-five adult male white outbred rats (200 ± 10 g) were housed under standard laboratory conditions (22 ± 2°C, 12 h light/dark cycle) with free access to food and water. All experimental procedures complied with institutional and international guidelines for the care and use of laboratory animals (EU Directive 2010/63/EU). MI was induced by permanent ligation of the left coronary artery under general anesthesia (ketamine/xylazine). The animals were observed for 72 hours, after which they were euthanized by decapitation.
Heart and liver tissues were rapidly excised, washed in ice-cold 0.15 M KCl, blotted, and weighed. Heart homogenates were prepared in a Teflon-glass homogenizer. Liver homogenates were pressed through a 0.5 mm mesh and homogenized in 0.05 M KCl (pH 7.4). Mitochondrial fractions were obtained by differential centrifugation (9000 g × 20 min), and microsomal fractions by ultracentrifugation (105,000 g ×60 min).
MDA concentration was determined by the TBARS method according to Stalnaya et al., and SOD activity by the method of Misra and Fridovich (modified by Brusov et al.). Data are expressed as mean ± SEM. Statistical comparisons were made using Student’s t-test, with p < 0.05 considered significant.
3. Results
Baseline measurements in control rats revealed relatively low MDA levels in cardiac tissue, consistent with a normal redox balance and minimal oxidative stress under physiological conditions. Significant, but stable, levels of lipid peroxidation products were observed in both mitochondrial (MF) and microsomal (MSF) liver fractions, reflecting basal membrane turnover and ROS generation typical for metabolic activity in healthy animals.
On day 3 post-MI, MDA levels rose sharply in all studied samples, indicating a marked activation of membrane lipid peroxidation. In cardiac homogenates, MDA concentration increased more than fivefold compared with controls (p < 0.01), demonstrating extensive oxidative damage to cardiomyocyte membranes. In the liver, MDA levels increased 6.1-fold in MF and an impressive 28.2-fold in MSF, suggesting that microsomal membranes were particularly vulnerable to ROS-induced peroxidation during systemic response to MI.
Table 1. MDA concentration in heart and liver fractions (control rats).

Tissue/Fraction

MDA (nmol/mg protein·min)

Ascorbate-Dependent Peroxidation (ADP)

NADH-Dependent Peroxidation (NDP)

ADP/NDP Ratio

Heart

1.65 ± 0.02

3.33 ± 0.11

6.71 ± 0.17

0.49 ± 0.03

Liver MF

8.10 ± 0.11

88.3 ± 0.73

64.5 ± 0.39

1.36 ± 0.11

Liver MSF

1.43 ± 0.06

11.2 ± 0.09

31.4 ± 0.29

0.35 ± 0.01
Post-MI Changes
On day 3 post-MI, MDA levels rose sharply (Table 2), indicating increased membrane lipid peroxidation.
Table 2. MDA concentration in cardiac tissue (3 days post-MI).

Group

MDA (nmol/mg protein·min)

ADP

NDP

ADP/NDP Ratio

Control

1.65 ± 0.02

3.33 ± 0.11

6.71 ± 0.17

0.49 ± 0.03

MI (Day 3)

7.42 ± 0.04

20.64 ± 0.14

82.53 ± 0.02

0.25 ± 0.02
Similar increases were observed in mitochondrial and microsomal fractions of the liver, with MSF showing the greatest change (Table 3).
Table 3. MDA concentration in liver fractions (3 days post-MI).

Fraction

Control

MI (Day 3)

Fold Increase

MF

8.10 ± 0.11

59.9 ± 1.73

×6.1

MSF

1.43 ± 0.06

28.8 ± 1.02

×28.2
In parallel with LPO activation, a significant suppression of the antioxidant defense system was observed. SOD activity declined by 31.5% in MF and by 73.1% in MSF (p < 0.01), indicating a profound weakening of the first-line enzymatic protection against superoxide radicals. This imbalance between excessive ROS generation and diminished antioxidant capacity reflects severe oxidative stress and may contribute to further propagation of cellular damage, not only in the myocardium but also in the liver as a key metabolic organ.
The combination of markedly elevated MDA and decreased SOD activity highlights a critical redox imbalance during the early post-infarction period, which may play a decisive role in the progression of myocardial injury and systemic complications.
4. Discussion
Our study demonstrates that experimental myocardial infarction (MI) in rats is accompanied by a pronounced activation of free radical lipid peroxidation (LPO) and a concomitant decrease in antioxidant enzyme activity. On day 3 post-MI, MDA levels in cardiac homogenates increased more than fivefold compared with controls, indicating severe oxidative damage to cardiomyocyte membranes. A similar pattern was observed in the liver, where MDA concentration rose 6.1-fold in the mitochondrial fraction (MF) and as much as 28.2-fold in the microsomal fraction (MSF). These findings confirm that MI induces not only local but also systemic oxidative stress, affecting organs distant from the primary ischemic site.
The observed decrease in superoxide dismutase (SOD) activity -31.5% in MF and 73.1% in MSF-suggests a significant depletion of antioxidant defenses. This is consistent with reports by other researchers showing that post-infarction oxidative stress is characterized by an imbalance between reactive oxygen species (ROS) production and detoxification capacity, leading to further propagation of cellular damage
[12]
.
Our results align with previous studies demonstrating that excessive ROS generation during MI can trigger lipid, protein, and nucleic acid oxidation, mitochondrial dysfunction, and eventual cell death. The particularly high vulnerability of microsomal membranes to peroxidation observed in our work may be explained by their structural and biochemical properties, including the presence of oxygen-dependent monooxygenase systems and high levels of polyunsaturated fatty acids, as noted in earlier biochemical studies
[18]
.
Taken together, these findings highlight oxidative stress as a key pathogenic factor in post-infarction myocardial remodeling and systemic metabolic disturbances. Our data, in agreement with literature reports, suggest that therapeutic modulation of redox status—via exogenous antioxidants, SOD mimetics, or mitochondrial stabilizers—could mitigate the extent of oxidative injury and improve recovery after MI. Future research should focus on standardizing experimental models to assess the efficacy of such interventions and to clarify their translational potential for clinical use.
5. Conclusion
Experimental myocardial infarction in rats causes a profound increase in lipid peroxidation and suppression of antioxidant defense mechanisms. These results support the utility of this model for studying cardioprotective interventions and screening antioxidant compounds.
Abbreviations

MI

Myocardial Infarction

ROS

Reactive Oxygen Species

LPO

Lipid Peroxidation

MDA

Malondialdehyde

SOD

Superoxide Dismutase

MF

Mitochondrial Fraction

MSF

Microsomal Fraction
Acknowledgments
The author expresses gratitude to Professor Zh. A. Rizaev, Rector of Samarkand State Medical University, for providing technical support to this work.
Author Contributions
Baykulov Azim Kenjayevich is the sole author. The author read and approved the final manuscript.
Funding
This work was not supported by any external funding.
Data Availability Statement
The data are available from the author upon request.
Conflicts of Interest
The author declares no conflicts of interest.
References
[1] Naveed, A., et al. Cardiovascular Diseases: Understanding the Leading Cause of Death Worldwide. Global Journal of Multi-disciplinary Sciences and Arts. 2021, 1(1), 100-110.
[2] Schupp, T., et al. Prognosis of cardiogenic shock with and without acute myocardial infarction: Results from a prospective, monocentric registry. Clinical Research in Cardiology. 2024, 113(4), 626-641.
[3] Tuka, V., Holub, J., Bělohlávek, J. Secondary prevention after myocardial infarction: What to do and where to do it. Reviews in Cardiovascular Medicine. 2022, 23(6), 210.
[4] Castiello, D. S., Polimeni, A., Curcio, A. Predictive value of scores for all-cause mortality in patients with cardiogenic shock. J Cardiovasc Med. 2025, 26, 280-283.
[5] Nasab, E. M., et al. COVID-19’s immuno-pathology and cardiovascular diseases. Journal of Investigative Medicine. 2023, 71(2), 71-80.
[6] Neves, K. B., et al. Exosomes and the cardiovascular system: Role in cardiovascular health and disease. The Journal of Physiology. 2023, 601(22), 4923-4936.
[7] Martin, T. P., et al. Preclinical models of myocardial infarction: From mechanism to translation. British Journal of Pharmacology. 2022, 179(5), 770-791.
[8] van Doorn, E. C. H., et al. Preclinical models of cardiac disease: A comprehensive overview for clinical scientists. Cardiovascular Engineering and Technology. 2024, 15(2), 232-249.
[9] Lindsey, M. L., et al. Guidelines for in vivo mouse models of myocardial infarction. American Journal of Physiology-Heart and Circulatory Physiology. 2021.
[10] Beyazcicek, E., Beyazcicek, O. Experimental myocardial infarction models and current approaches. Current studies in basic medical sciences. Lyon: Livre de Lyon; 2023, pp. 55-76.
[11] Filippo, C. D., et al. Oxidative stress as the leading cause of acute myocardial infarction in diabetics. Cardiovascular Drug Reviews. 2006, 24(2), 77-87.
[12] Zeng, J., et al. Effect of lipid oxidation on quality attributes and control technologies in dried aquatic animal products: A critical review. Critical Reviews in Food Science and Nutrition. 2023, 1-22.
[13] Whitworth, G. B., Watson, F. L. Translating Ribosome Affinity Purification (TRAP) and Bioinformatic RNA-Seq Analysis in Post-metamorphic Xenopus laevis. In: Axon Regeneration: Methods and Protocols. New York, NY: Springer US; 2023, pp. 279-310.
[14] Acín-Pérez R., et al. Isolation of mitochondria from mouse tissues for functional analysis. In: Metabolic Reprogramming: Methods and Protocols. New York, NY: Springer; 2023. pp. 77–96.
[15] Kenjayevich B.A., Baxriddinovna U.G. Dynamics of the nitrergic system in experimental hypercholesterolemia. Education News: Research in the 21st Century. 2023; 1(9): 1452–1458
[16] Varesi, A., et al. The role of antioxidants in the interplay between oxidative stress and senescence. Antioxidants. 2022, 11(7), 1224.
[17] Baykulov, A. K., Norberdiyev, S. S. Eksperimental giperxolesterolemiyada qondagi gomosistein miqdori bilan endoteliy disfunktsiyasi bog‘liqligi. Educational Research in Universal Sciences. 2023, 2(3), 396-402.
[18] Lesnefsky, E. J., Moghaddas, S., Tandler, B., et al. Mitochondrial dysfunction in cardiac disease: Ischemia-reperfusion, aging, and heart failure. J Mol Cell Cardiol. 2001, 33(6), 1065-1089. HYPERLINK "

https://doi.org/10.1006/jmcc.2001.1378" https://doi.org/10.1006/jmcc.2001.1378

Cite This Article
Plain Text BibTeX RIS

  • APA Style

    Kenjayevich, B. A. (2026). Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue. International Journal of Cardiovascular and Thoracic Surgery, 12(1), 14-17. https://doi.org/10.11648/j.ijcts.20261201.13

    Copy | Download

    ACS Style

    Kenjayevich, B. A. Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue. Int. J. Cardiovasc. Thorac. Surg. 2026, 12(1), 14-17. doi: 10.11648/j.ijcts.20261201.13

    Copy | Download

    AMA Style

    Kenjayevich BA. Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue. Int J Cardiovasc Thorac Surg. 2026;12(1):14-17. doi: 10.11648/j.ijcts.20261201.13

    Copy | Download 

  • @article{10.11648/j.ijcts.20261201.13,
  author = {Baykulov Azim Kenjayevich},
  title = {Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue},
  journal = {International Journal of Cardiovascular and Thoracic Surgery},
  volume = {12},
  number = {1},
  pages = {14-17},
  doi = {10.11648/j.ijcts.20261201.13},
  url = {https://doi.org/10.11648/j.ijcts.20261201.13},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcts.20261201.13},
  abstract = {Introduction: Myocardial infarction (MI) remains one of the most common and life-threatening cardiovascular diseases worldwide. Experimental models of MI are essential for understanding its pathophysiology and evaluating therapeutic interventions. Objective: The aim of this study was to evaluate lipid peroxidation and antioxidant defense during experimental MI in rats. Methods: MI was induced in adult male rats by ligation of the left coronary artery. On the third day after MI, cardiac and liver tissues were collected. Heart and liver homogenates, as well as mitochondrial (MF) and microsomal (MSF) fractions of the liver, were analyzed for malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity. Results: Compared with the control group, MDA concentration increased fivefold in cardiac homogenates and 6.1-fold in liver MF, while MSF showed the most pronounced increase (28.2-fold). SOD activity was significantly reduced: by 31.5% in MF and by 73.1% in MF. Conclusion: Experimental MI induces pronounced oxidative stress, characterized by excessive lipid peroxidation and suppression of antioxidant defenses. This model represents a valuable tool for investigating cardioprotective strategies and antioxidant therapy.},
 year = {2026}
}

    Copy | Download 

  • TY  - JOUR
T1  - Oxidative Stress and Lipid Peroxidation in Experimental Myocardial Infarction: Biochemical Evaluation in Cardiac and Hepatic Tissue
AU  - Baykulov Azim Kenjayevich
Y1  - 2026/02/02
PY  - 2026
N1  - https://doi.org/10.11648/j.ijcts.20261201.13
DO  - 10.11648/j.ijcts.20261201.13
T2  - International Journal of Cardiovascular and Thoracic Surgery
JF  - International Journal of Cardiovascular and Thoracic Surgery
JO  - International Journal of Cardiovascular and Thoracic Surgery
SP  - 14
EP  - 17
PB  - Science Publishing Group
SN  - 2575-4882
UR  - https://doi.org/10.11648/j.ijcts.20261201.13
AB  - Introduction: Myocardial infarction (MI) remains one of the most common and life-threatening cardiovascular diseases worldwide. Experimental models of MI are essential for understanding its pathophysiology and evaluating therapeutic interventions. Objective: The aim of this study was to evaluate lipid peroxidation and antioxidant defense during experimental MI in rats. Methods: MI was induced in adult male rats by ligation of the left coronary artery. On the third day after MI, cardiac and liver tissues were collected. Heart and liver homogenates, as well as mitochondrial (MF) and microsomal (MSF) fractions of the liver, were analyzed for malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity. Results: Compared with the control group, MDA concentration increased fivefold in cardiac homogenates and 6.1-fold in liver MF, while MSF showed the most pronounced increase (28.2-fold). SOD activity was significantly reduced: by 31.5% in MF and by 73.1% in MF. Conclusion: Experimental MI induces pronounced oxidative stress, characterized by excessive lipid peroxidation and suppression of antioxidant defenses. This model represents a valuable tool for investigating cardioprotective strategies and antioxidant therapy.
VL  - 12
IS  - 1
ER  -

    Copy | Download

Author Information
Download PDF
Submit an Article

About Us

Science Publishing Group (SciencePG) is an Open Access publisher, with more than 300 online, peer-reviewed journals covering a wide range of academic disciplines.

Learn More About SciencePG

Products

Information

Important Link

Copyright © 2012 -- 2026 Science Publishing Group – All rights reserved.