ArticleJournal of medical biochemistry2026
Neutrophil redox imbalance in acute coronary syndrome.
Article in Journal of medical biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Background: Oxidative stress contributes significantly to the pathogenesis of acute coronary syndrome (ACS), with neutrophils playing a pivotal role in mediating vascular injury through reactive oxygen species and myeloperoxidase (MPO)-derived oxidants. We aimed to assess the oxidative stress markers and antioxidant enzyme activities in neutrophils from ACS patients. Methods: Neutrophils were isolated from 77 ACS patients and 33 control subjects. Oxidative stress was evaluated by measuring conjugated dienes, hydroperoxides, and chloramines. Antioxidant status was assessed via non-protein and total thiol levels, and enzymatic activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx-1), and glutathione reductase (GR). MPO peroxidase and chlorinating activities were also quantified. Results: ACS patients exhibited significantly elevated levels of conjugated dienes (p< 0.005), chloramines (p< 0.005), thiols (p< 0.05), SOD activity (p= 0.01), and MPO chlorinating activity (p< 0.05). No significant differences were observed in catalase, GPx-1, GR, or MPO peroxidase activity. Significant correlations were found between lipid peroxidation markers and antioxidant parameters, particularly SOD and MPO chlorinating activity. Multiple regression identified SOD and chloramines as independent predictors of lipid peroxidation. Conclusions: Neutrophils from ACS patients display a disrupted redox balance characterised by enhanced lipid peroxidation, increased thiol content, and selective activation of MPO chlorination. These results underscore the relevance of neutrophil-derived redox markers as potential diagnostic tools and treatment targets in ACS.
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