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Benign prostatic hyperplasia (BPH), chronic prostatitis (CP), and prostate cancer (PC) are frequently occurring conditions that affect the prostate gland, with overlapping clinical features and potentially shared pathogenetic mechanisms. A growing body of research indicates that oxidative stress (OS) is a critical factor in both the onset and advancement of these disorders. Xanthine oxidase (XO) is a known enzymatic source of reactive oxygen species (ROS), however, its involvement in prostate disease pathogenesis remains underexplored.
The study included 17 patients with CP, 10 with BPH, and 15 with PC. Ten healthy individuals served as controls. Serum samples were collected for BPH and CP groups, while PC samples were obtained from surgical tissues. OS was assessed by measuring thiobarbituric acid-reactive substances (TBARS) and advanced oxidation protein products (AOPP). XO activity was determined spectrophotometrically in plasma and tissue homogenates.
Serum concentrations of TBARS and AOPP were markedly higher in individuals diagnosed with BPH and CP relative to those in the healthy control group (p < 0.001). Similarly, XO activity was markedly increased in these groups. In PC tissue, both TBARS and AOPP concentrations, as well as XO activity, were significantly higher than in non-tumor prostate tissue (p < 0.001), indicating local OS and enzymatic ROS production.
These findings confirm that systemic and tissue-level OS is elevated in BPH, CP, and PC. XO may represent a shared mechanism linking inflammation and carcinogenesis. The study supports further investigation into the therapeutic potential of antioxidants and XO inhibitors as adjunct strategies in prostate disease management.

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