DOI : https://doi.org/10.18517/ijaseit.15.1.20826

Modulation of Oxidative Stress Markers and Inflammatory Mediators in Alveolar Damage Induced by Anaerobic Exercise

Siti Khotimah (1), Muchsin Doewes (2), Reviono Reviono (3), Brian Wasita (4), Bambang Purwanto (5), Soetrisno Soetrisno (6), Eti P. Pamungkasari (7), Paramasari Dirgahayu (8)
(1) Doctoral Program of Medical Sciences, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia
(2) Doctoral Program of Medical Sciences, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia
(3) Doctoral Program of Medical Sciences, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia
(4) Doctoral Program of Medical Sciences, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia
(5) Doctoral Program of Medical Sciences, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia
(6) Doctoral Program of Medical Sciences, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia
(7) Doctoral Program of Medical Sciences, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia
(8) Doctoral Program of Medical Sciences, Faculty of Medicine, Universitas Sebelas Maret, Surakarta, Indonesia
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S. Khotimah, “Modulation of Oxidative Stress Markers and Inflammatory Mediators in Alveolar Damage Induced by Anaerobic Exercise”, Int. J. Adv. Sci. Eng. Inf. Technol., vol. 15, no. 1, pp. 267–274, Feb. 2025.
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Anaerobic exercise, characterized by high-intensity, short-duration physical activity, induces a unique physiological response that includes oxidative stress and inflammation. This study investigates the modulation of oxidative stress markers and inflammatory mediators in alveolar damage induced by anaerobic exercise. Key parameters, including superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, and tumor necrosis factor-alpha (TNF-α), were analyzed to elucidate their roles in oxidative and inflammatory pathways. Using rats as an experimental model, subjects were exposed to an 8-week anaerobic training regimen, and alveolar tissue samples were evaluated for oxidative stress and inflammatory markers. Histopathological changes and biochemical markers were analyzed across treatment groups and three time points (D-20, D-40, D-60). Results demonstrated a significant group- and time-dependent variations were observed in MDA, SOD, and TNF levels. The MDA levels was high, indicative of lipid peroxidation, while SOD showed elevated oxidative burden across treatment groups. TNF levels were consistently higher in the treatment group, highlighting its role in inflammation. Temporal analyses revealed stabilization at D-40 for certain markers, followed by significant increases at D-60. Correlation analyses indicated strong positive relationships between histopathology and oxidative stress markers, while TNF exhibited a dual role, correlating positively with oxidative stress but negatively with histopathological damage. The findings underscore the multifactorial nature of alveolar damage, driven by the interplay between oxidative stress and inflammation. The interaction network highlights the interconnected roles of MDA, SOD, TNF, and histopathological damage.

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