Elevated plasma molybdenum level increases the risk of premature ovarian insufficiency through vascular endothelial injury.

This article investigates the association between elevated plasma molybdenum levels and idiopathic premature ovarian insufficiency (POI), a condition characterized by early ovarian dysfunction in women under 40. A case-control study of 30 women with idiopathic POI and 31 controls found higher plasma molybdenum and calcium concentrations in POI patients, with statistical analyses indicating a synergistic interaction increasing POI risk. Experimental studies in mice and human cell lines demonstrated that molybdenum exposure induces vascular endothelial injury by enhancing nitric oxide generation and calcium influx, leading to increased ovarian vascular permeability, platelet activation, and serotonin release; serotonin then induces granulosa cell quiescence, while molybdenum directly inhibits granulosa cell proliferation via downregulation of isocitrate dehydrogenase 1 (IDH1). These findings suggest that excessive plasma molybdenum contributes to ovarian dysfunction through vascular and cellular mechanisms, highlighting molybdenum as a potential risk factor for idiopathic POI, though further large-scale studies are needed to confirm these results and clarify the source of molybdenum elevation.