Background Endometriosis is a chronic inflammatory and estrogen-dependent disorder associated with oxidative stress, immune dysregulation, and altered trace-element homeostasis. This study investigated the association between serum trace elements, oxidative-stress biomarkers, and inflammatory cytokines in women with endometriosis, with particular emphasis on their interplay in disease pathophysiology and their potential utility for integrated biomarker profiling. Materials and Methods A total of 120 women, comprising 60 women with endometriosis and 60 healthy controls, were enrolled. Serum concentrations of trace elements (As, Pb, Cd, Hg, Cu, Fe, Zn, and Se) were measured using graphite furnace atomic absorption spectrophotometry. Oxidative-stress biomarkers (MDA, SOD, glutathione, and 8-OHdG) and inflammatory cytokines (TNF-α, TGF-β, IFN-γ, IL-6, IL-1β, and IL-10) were assessed using ELISA-based methods. Data distribution was assessed using the Shapiro–Wilk test before group comparisons. Trace-element and oxidative-stress biomarkers showed non-normal distributions and were analyzed using the Mann–Whitney U test, whereas inflammatory cytokine variables met normality assumptions and were analyzed using the unpaired Student’s t-test. Associations among biomarkers were evaluated using Spearman’s rank correlation analysis. Results Women with endometriosis exhibited significantly higher serum levels of As, Pb, Hg, Cu, and Fe and significantly lower Zn and Se levels compared with healthy controls. Oxidative-stress profiling demonstrated significantly increased MDA, SOD, and 8-OHdG levels and significantly reduced glutathione levels in the endometriosis group ( p < 0.001). Inflammatory profiling revealed significantly elevated TNF-α, IL-6, IL-1β, and IL-10 levels, whereas IFN-γ was significantly reduced; TGF-β showed a non-significant increasing trend. Spearman’s correlation analysis identified selective associations among trace elements, oxidative-stress biomarkers, and inflammatory cytokines, including positive correlations of Cu with IL-1β and As with TGF-β, and a negative correlation of Fe with glutathione. Conclusion Women with endometriosis demonstrated coordinated alterations in trace-element status, redox homeostasis, and inflammatory signaling. The observed associations suggest an interconnected redox-inflammatory phenotype that may contribute to the biological stress environment associated with endometriosis. These findings support further investigation of trace-element and oxidative-stress profiles as potential biomarkers of disease-related biological alterations, while larger multicenter and longitudinal studies are needed to establish their clinical relevance and causal relationships.
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Ashish et al. (2026) studied this question.
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