Post-transcriptional RNA regulation is critical for the formation of primordial follicles, which determine female reproductive potential. Stress-induced disruptions in RNA metabolism are increasingly recognized as key factors impairing oogenesis, but the underlying mechanisms remain poorly understood. Here, we reveal that maternal exposure to aristolochic acid I (AAI), a reproductive toxicant commonly found in traditional medicines, disrupts P-body (PB) dynamics in neonatal mouse oocytes, resulting in impaired RNA metabolism during early folliculogenesis. These alterations contribute to defective primordial follicle formation and compromised oocyte competence in adulthood, ultimately compromising female fertility. Specifically, we identify NANOS3 and YTHDF2 as critical mediators of PB assembly, orchestrating RNA stabilization and degradation in response to AAI. Our findings demonstrate that YTHDF2, the m6A reader, facilitates the recruitment of NANOS3 to PBs, modulating the composition and functionality of these membraneless organelles. Proteomic analyses reveal that AAI induces aberrant associations of RNA-processing proteins with DDX6, a core PB component, altering the fate of transcripts with m6A modification during primordial follicle formation. This study highlights a mechanistic link between stress-induced PB assembly and RNA metabolism, providing new insights into how environmental factors influence female reproductive health. By uncovering the molecular basis of these processes, our work underscores the importance of RNA-centric regulatory networks in oogenesis and their vulnerability to external stressors.