Cutaneous and ocular toxicology · 2025
Systemic oxidative stress imbalance in actinic keratosis: Insights from thiol-disulfide homeostasis and ischemia-modified albumin.
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Metin Mahmut Sami, Demirbaş Abdullah, Diremsizoglu Esin, Tehçi Tuğba, Kolukırık İlkay, Akoğul Serkan, Metin Zühal, Özkoca Defne, Neşelioğlu Salim, Erel Özcan
Аннотация
BACKGROUND: Actinic keratosis (AK) is a common premalignant skin condition linked to chronic ultraviolet (UV) exposure and oxidative stress. Systemic biomarkers of redox imbalance in AK remain underexplored.
AIMS: To assess systemic oxidative stress in AK using plasma thiol-disulfide homeostasis (TDH) and ischemia-modified albumin (IMA).
METHODS: This cross-sectional study included 42 patients with clinically diagnosed AK and 42 age- and sex-matched healthy controls. Native thiol, total thiol, disulfide concentrations, and derived redox indices (Index-1, -2, -3) were measured using a spectrophotometric assay. IMA levels were assessed via the albumin-cobalt binding test. Statistical comparisons and correlation analyses were performed.
RESULTS: Native thiol, total thiol, and disulfide levels were significantly lower in the AK group (p = 0.001), whereas disulfide-based indices showed no significant differences. IMA concentrations were significantly elevated in AK patients (p = 0.001). IMA levels were negatively correlated with native (r = -0.312, p = 0.044) and total thiol (r = -0.309, p = 0.046) values. Patients with Fitzpatrick Type IV skin exhibited significantly higher lesion counts than those with Types II and III (p < 0.05).
CONCLUSION: AK patients show systemic oxidative imbalance, with reduced thiols and elevated IMA, reflecting persistent UV-induced redox stress and protein oxidation. TDH and IMA may have potential utility as systemic indicators of oxidative stress in AK. Limitations include cross-sectional design, modest sample size, and unmeasured confounders. Future longitudinal and interventional studies should assess causality and antioxidant-based therapies.
AIMS: To assess systemic oxidative stress in AK using plasma thiol-disulfide homeostasis (TDH) and ischemia-modified albumin (IMA).
METHODS: This cross-sectional study included 42 patients with clinically diagnosed AK and 42 age- and sex-matched healthy controls. Native thiol, total thiol, disulfide concentrations, and derived redox indices (Index-1, -2, -3) were measured using a spectrophotometric assay. IMA levels were assessed via the albumin-cobalt binding test. Statistical comparisons and correlation analyses were performed.
RESULTS: Native thiol, total thiol, and disulfide levels were significantly lower in the AK group (p = 0.001), whereas disulfide-based indices showed no significant differences. IMA concentrations were significantly elevated in AK patients (p = 0.001). IMA levels were negatively correlated with native (r = -0.312, p = 0.044) and total thiol (r = -0.309, p = 0.046) values. Patients with Fitzpatrick Type IV skin exhibited significantly higher lesion counts than those with Types II and III (p < 0.05).
CONCLUSION: AK patients show systemic oxidative imbalance, with reduced thiols and elevated IMA, reflecting persistent UV-induced redox stress and protein oxidation. TDH and IMA may have potential utility as systemic indicators of oxidative stress in AK. Limitations include cross-sectional design, modest sample size, and unmeasured confounders. Future longitudinal and interventional studies should assess causality and antioxidant-based therapies.