Liver Function as a Determinant of Antioxidant Therapeutic Efficacy in Benign Prostatic Hyperplasia: A Systems Biology Perspective

Benign Prostatic Hyperplasia (BPH) is a non-malignant enlargement of the prostate gland predominantly affecting aging males. While oxidative stress (OS) is recognized as a key pathogenic driver in BPH, emerging evidence highlights the liver’s critical role in modulating systemic redox homeostasis and influencing antioxidant therapeutic responses. Liver function not only governs the bioavailability, metabolism, and clearance of antioxidant compounds but also contributes to systemic inflammation and metabolic alterations that exacerbate BPH pathophysiology. This review adopts a systems biology approach to explore the complex liver-prostate axis, emphasizing how liver health determines the pharmacokinetics, pharmacodynamics, and therapeutic efficacy of antioxidant interventions in BPH management. We discuss the molecular mechanisms underpinning hepatic regulation of antioxidant bioactivity, the impact of liver dysfunction on BPH progression, and emerging therapeutic strategies aimed at restoring liver-prostate homeostasis. Future research directions advocate for precision antioxidant therapy guided by liver function biomarkers, systems biology modeling, and integrative metabolic profiling. Keywords: Benign Prostatic Hyperplasia; Liver Function; Antioxidant Therapy; Oxidative Stress; Systems Biology