Exposure to diethyl phthalates impairs ovarian reserve and oocyte maturation in female mice.

Diethyl phthalates (DEP) are commonly used as a plasticizer and have been found to cause male reproductive defects and metabolic disease in mammals as a potential environmental endocrine disruptor. However, the effects and underlying mechanisms of DEP exposure on female follicle development and oocyte maturation were still unclear. In this study, we found that mice exposed to DEP had significantly reduced primordial follicles. DEP exposure also led to a decrease in the number of ovulated oocytes, the rate of the first polar body, and an increase in fragmentation. Transcriptome analysis showed significant changes in the transcription levels of genes related to the actin filament, reproduction, post-translational protein modification, PI3K-AKT, TGF-beta, Wnt signaling pathway, and mitochondria function. Furthermore, over ten differentially expressed genes in DEP-exposed mice overlapped with 703 genes related to ovarian function from patients with premature ovarian insufficiency (POI). In conclusion, our study demonstrates that DEP exposure can impair primordial follicle number and oocyte maturation competence by affecting mitochondria distribution and function. This study sheds light on the possible effects of plastic additives on female reproductive health and offers potential strategies for the prevention and treatment of infertility related to these additives.