Systemic Oxidative and Nitrosative Stress in Benign Prostatic Hyperplasia

Benign prostatic hyperplasia (BPH) is an age-related disorder increasingly linked to chronic inflammation and redox imbalance, yet its systemic oxidative and nitrosative profile remains insufficiently characterized. In this cross-sectional study, fasting serum samples were collected from 47 men with clinically confirmed BPH scheduled for transurethral resection of the prostate and 40 healthy controls. We assessed antioxidant status (thiols, total antioxidant capacity), lipid peroxidation (malondialdehyde, 4-hydroxynonenal), protein nitration (3-nitrotyrosine), glycoxidation markers (Amadori products, advanced glycation end products (AGE)-associated fluorescence), and tryptophan metabolism indices (tryptophan, kynurenine, N′-formylkynurenine). Compared with controls, BPH patients showed significantly lower antioxidant capacity and thiol levels, together with increased lipid peroxidation and protein nitration. AGE-associated fluorescence was modestly elevated, whereas Amadori products and advanced oxidation protein products did not differ significantly. Tryptophan metabolism was markedly altered, with lower tryptophan and higher kynurenine and N′-formylkynurenine, indicating activation of the kynurenine pathway. After false discovery rate correction, most redox biomarkers remained significant. Multivariable logistic regression confirmed independent associations of lipid peroxidation, nitrosative stress, and kynurenine pathway activation with BPH after adjustment for age and metabolic parameters. These findings support a role for systemic oxidative and inflammatory mechanisms in BPH pathophysiology, although confirmation in age-matched and longitudinal studies is needed.