Protective effects of naringenin and naringin against bisphenol A-induced male reproductive toxicity: mechanistic and preclinical evidence.

Bisphenol A (BPA) has been associated with altered male reproductive hormones and semen endpoints in epidemiological studies and produces endocrine, oxidative, mitochondrial, apoptotic, and developmental injury in experimental models. This narrative review evaluates BPA-specific evidence for naringenin and naringin separately from supportive evidence in other reproductive stress models. It also distinguishes directly exposed F1 outcomes from transgenerational inheritance and links sperm endpoints to hormones, histology, and molecular measures. This narrative review synthesizes evidence published mainly between January 2019 through September 2026, while retaining older studies of direct mechanistic relevance. Evidence was identified through targeted searches of PubMed, Scopus-indexed sources, Google Scholar, and publisher databases and was organized by exposure timing, biological mechanism, model type, and reproductive endpoint. The strongest evidence for BPA-related male reproductive toxicity comes from convergent cellular and animal data supported by heterogeneous human observational studies. The strongest evidence for naringenin or naringin is preclinical and includes BPA-specific Sertoli-cell and rat models as well as related oxidative, metabolic, and phthalate stress models. Across the broader preclinical literature, the flavanones modify redox, mitochondrial, inflammatory, and steroidogenic endpoints, but differences in model, dose, route, and bioavailability prevent quantitative comparison. The evidence supports mechanistic research, not clinical supplementation, and exposure reduction remains the primary public-health approach.