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While previous studies have demonstrated that prenatal exposure to SiO<jats:sub>2<\/jats:sub> NPs can traverse the placental barrier and induce neurotoxicity in offspring. However, their reproductive toxicity remains unclear. Here, it is found that prenatal SiO<jats:sub>2<\/jats:sub> NPs exposure led to subfertility in female offspring, evidenced by decreased ovulation potential, ovarian reserve, and litter size. In contrast, male offspring maintained normal sperm production and fertility. Mechanistic analyses revealed that prenatal SiO<jats:sub>2<\/jats:sub> NPs exposure disrupted meiotic recombination and increased oocyte apoptosis, resulting in reduced postnatal primordial follicle formation in females. Conversely, meiotic recombination occurring postnatally in male offspring remained unaffected. Notably, treatment with carboxylate (COOH)\u2010functionalized SiO<jats:sub>2<\/jats:sub> nanoparticles (SiO<jats:sub>2<\/jats:sub>\u2010COOH NPs) has a minimal impact on fertility in female offspring. Further research, including clinical studies, is needed to confirm these findings in humans. 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