Long-term and low-dose exposure to triclosan induces POI phenotype in female offspring mice.

Triclosan (TCS), a typical endocrine disruptor, is widely used as an antibacterial agent in consumer goods. However, there are few studies on the effects of long-term low-dose TCS exposure on ovarian function in F1 female mice. In this paper, F1 female mice were exposed to TCS (0-3000 μg/kg/day) from intrauterine to postnatal day (PND) 91 to investigate its effects on the ovary. The results revealed that the number of total follicles was decreased, while atretic follicles was increased after TCS exposure. At the hormonal level, the secretion of estradiol was reduced, while follicle-stimulating hormone and luteinizing hormone were increased after TCS exposure. Observation of vaginal smear showed that TCS disrupted the estrous cycle of F1 female mice, especially at the dose of 3000 μg/kg/day. Moreover, TCS promoted cell apoptosis by activating the p38-MAPK signaling pathway and oxidative stress in vitro. In addition, analysis of the fecal microbiome and serum metabolomics revealed that exposure to TCS may cause gut microbiota disruption and metabolic abnormalities in F1 female mice. In conclusion, long-term low-dose TCS exposure may induce primary ovarian insufficiency phenotype in F1 female mice via inducing cell apoptosis and disrupting gut microbiota and metabolism.