Bisphenols and follicle function in farm species

Bisphenols are synthetic chemicals widely used in the production of plastics, resins, and food-contact materials, resulting in ubiquitous environmental exposure in humans and animals. Among their biological effects, increasing evidence highlights their ability to disrupt ovarian function. This review synthesizes current knowledge on the impact of bisphenols and their analogues on ovarian follicle physiology in domestic species, drawing primarily from bovine, ovine, and porcine studies, with comparisons to human and rodent data. After outlining bisphenol structures, exposure routes, and metabolic pathways in farm animals, we summarize their mechanisms of action on follicular cells, including receptor-mediated signaling, transcriptional regulation, epigenetic modifications, oxidative stress, and apoptosis. Experimental data consistently indicate that bisphenols alter key ovarian processes such as folliculogenesis, steroidogenesis, granulosa cell viability, oocyte maturation, and embryo development. However, the magnitude and direction of these effects vary depending on the compound, dose, exposure duration, and experimental model. A major emerging factor influencing bisphenol sensitivity is the metabolic status of the exposed animal. Evidence suggests that nutritional or metabolic imbalances modulate ovarian responses to bisphenols, potentially through interactions between metabolic and endocrine pathways involving estrogen receptors (ERs), thyroid hormone receptor (TR), glucocorticoid receptor (GR), and peroxisome proliferator-activated receptors (PPARs). Future research should integrate reproductive and metabolic endpoints to better elucidate the mechanisms underlying bisphenol-induced ovarian dysfunction under physiologically relevant conditions. Such approaches are essential for assessing the reproductive risks of chronic, low-dose exposure to bisphenols in livestock and for supporting sustainable animal production systems.