Mieloperoxidasa como indicador de estrés oxidativo en síndrome metabólico

pp 514-518

Authors

  • María L. Garagiola Chair of Biomedical Physics. School of Medicine, Universidad Nacional de Córdoba.
  • Mariana Tarán Chair of Biomedical Physics. School of Medicine, Universidad Nacional de Córdoba.
  • María P. Scribano Chair of Biomedical Physics. School of Medicine, Universidad Nacional de Córdoba.
  • Ariel Balceda Chair of Biomedical Physics. School of Medicine, Universidad Nacional de Córdoba.
  • Emilia García Chair of Biomedical Physics. School of Medicine, Universidad Nacional de Córdoba.
  • Ismael Fonseca II Chair of Anatomy Pathology, Facultad de Ciencias médicas. Universidad Nacional de Córdoba. FINANCIAL SUPPORT:- Secretariat of Science and Technology (SECYT) of Universidad Nacional de Córdoba - Science and Technology (CYCYT) of Universidad Nacional de La Rioja - PID 2010, MINCYT, Ministry of Industry of the Province of Córdoba
  • Mónica Moya Chair of Biomedical Physics. School of Medicine, Universidad Nacional de Córdoba. -Biomedical Physics. School of Medicine, Universidad Nacional de La Rioja.
  • María C. Baez Chair of Biomedical Physics. School of Medicine, Universidad Nacional de Córdoba. -Física Biomédica. Facultad de Medicina, Universidad Nacional de La Rioja.Biomedical Physics. School of Medicine, Universidad Nacional de La Rioja.

DOI:

https://doi.org/10.7775/rac.v84i6.1270

Keywords:

Myeloperoxidase, Oxidative Stress, Metabolic Syndrome, Insulin Resistance, Cardiovascular Risk

Abstract

Background: Increased myeloperoxidase (MPO) activity would be the link between the rise of the inflammatory response and oxidative stress (OS) in metabolic syndrome (MS).
Objective: The aim of this study was to determine the enzymatic activity of MPO associated with OS in animals with MS and establish their relationship with probable cardiovascular injury.
Methods: Male Wistar rats were divided into two groups: Group A, control (n=12) and Group B, induced MS (n=12). Metabolic syndrome was produced by 6-week administration of 10% fructose diluted in the drinking water. Insulin (μU/ml), glucose (mg/dl), lipid panel (mg/dl), HOMA (homeostatic model assessment), MPO (IU/ml) and superoxide dismutase (SOD) activity (U/ml) were measured. Light microscopy was used for the histological study of the heart and thoracic aorta.
Results: Group B showed significantly increased levels of plasma glucose (176±17.3 mg/dl), insulin (29.5±4.52 μU/ml), HOMA(11±1.3), total cholesterol (133±9.6 mg/dl) and triglycerides (75±12.9 mg/dl) compared with Group A: plasma glucose (115±1.1
mg/dl), insulin (4±0.82 μU/ml), HOMA (3±0.38), total cholesterol (69.7±1.6 mg/dl) and triglycerides (46.2±6 mg/dl), (p<0.001 for all variables). A significant decrease in HDL (28.3±1.14 mg/dl) in Group B vs. Group A (61±1.0 mg/dl) (p<0.001) validated the experimental MS model. Myeloperoxidase activity increased significantly in Group B (181.3±15.7 IU/ml) vs. Group A (116.07±4.2 IU/ml) (p<0.001). A similar behavior was seen with SOD antioxidant activity in Group B (181±6 U/ml) vs. Group A (138±3.6 U/ml) (p<0.01). Light microscopy of the heart and thoracic aorta revealed histopathological changes in animals with induced MS.
Conclusion: Increased MPO and SOD in Group B would indicate the presence of OS in MS, with consequences at the vascular level.

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Published

2025-09-02

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ORIGINAL ARTICLES

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