Mitochondrial DNA copy number as a biomarker of oxidative stress and inflammation in premature ovarian insufficiency.

To examine how mitochondrial DNA copy number (mtDNAcn) relates to oxidative stress and persistent inflammation in individuals with premature ovarian insufficiency (POI). A single-center case-control investigation, spanning January 2020 to December 2022, recruited 100 POI patients alongside 100 healthy volunteers at our institution. We evaluated baseline demographic and clinical traits across both cohorts. Using qPCR, we quantified mtDNAcn in peripheral blood, while ELISA measured serum markers of oxidative stress (reactive oxygen species [ROS], superoxide dismutase [SOD], glutathione S-transferase [GST]) and inflammatory cytokines (tumor necrosis factor-α [TNF-α], interferon-γ [IFN-γ], interleukin-1β [IL-1β], interleukin-10 [IL-10], transforming growth factor-β [TGF-β]). We applied ROC curve analysis to gauge mtDNAcn's diagnostic potential for POI, with Pearson correlation and multiple linear regression exploring links to oxidative and inflammatory factors. No notable differences emerged in age, body mass index, blood pressure, parity, gravidity, or menarche onset (P > 0.05). POI patients displayed elevated serum TNF-α, IFN-γ, IL-1β, and ROS, but reduced IL-10, TGF-β, SOD, GST, and mtDNAcn (P < 0.05). Exploratory ROC analysis suggested that mtDNAcn had good predictive capacity in this single-center cohort (AUC = 0.951, 95% CI: 0.922-0.980). mtDNAcn positively associated with IL-10, TGF-β, SOD, and GST, yet inversely with TNF-α, IFN-γ, IL-1β, and ROS (P < 0.05). Multiple linear regression identified these markers as independently associated with mtDNAcn. Lower mtDNAcn in peripheral blood of POI patients was associated with increased oxidative stress and chronic inflammation. mtDNAcn may serve as a potential non-invasive biomarker candidate for POI, but prospective studies with external validation are required to establish its clinical utility.