Birth defects research · 2026
Potential Effects of Prepubertal Exposure to Perfluorooctane Sulfonic Acid on the First Wave of Folliculogenesis in Young CD-1 Mice.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Phanavanh Bounleut, Moore Jalina, Inselman Amy, Li Xiaoqing, Sung Kyung, Hung Pei-Hsuan, You Li, Nakamura Noriko
Аннотация
BACKGROUND: Perfluorooctane sulfonic acid (PFOS) belongs to a group of synthetic chemicals referred to as per- and polyfluoroalkyl substances (PFAS) that are known to degrade slowly. Exposure to PFOS has been reported to cause birth defects and disrupt female sex hormone levels in mice. However, to date, the direct effects of PFOS exposure on folliculogenesis in young animals have not been evaluated. Therefore, this study was conducted to examine the potential effects of in utero and prepubertal exposure to PFOS on follicle development in juvenile, female mouse pups.
METHODS: ICR dams and young, female mouse pups were dosed with 0.1 mg/kg PFOS or saline (vehicle) via gavage beginning on gestation day (GD) 6 (plug positive = GD 0) through GD 17 (n = 11-17 per group) [in utero exposure] or postnatal day (PND) 7 (PND 0 = day of birth) through PND 21 (n = 22-29 per group) [prepubertal exposure]. Ovaries and blood were then collected from a pup/litter on PND 28 for analysis.
RESULTS: There were no adverse effects of PFOS exposure observed in the measured endpoints upon in utero exposure; however, statistically significant differences following prepubertal exposure were noted for serum estradiol levels, the total number of primordial follicles, and the transcript levels of Foxo1 and Gdf9.
CONCLUSION: The preliminary findings suggest that prepubertal exposure to PFOS may affect follicle development by disrupting estradiol production and altering Foxo1 and Gdf9 gene expression. Further studies will be important to examine the mechanisms underlying prepubertal exposure to PFOS on folliculogenesis.
METHODS: ICR dams and young, female mouse pups were dosed with 0.1 mg/kg PFOS or saline (vehicle) via gavage beginning on gestation day (GD) 6 (plug positive = GD 0) through GD 17 (n = 11-17 per group) [in utero exposure] or postnatal day (PND) 7 (PND 0 = day of birth) through PND 21 (n = 22-29 per group) [prepubertal exposure]. Ovaries and blood were then collected from a pup/litter on PND 28 for analysis.
RESULTS: There were no adverse effects of PFOS exposure observed in the measured endpoints upon in utero exposure; however, statistically significant differences following prepubertal exposure were noted for serum estradiol levels, the total number of primordial follicles, and the transcript levels of Foxo1 and Gdf9.
CONCLUSION: The preliminary findings suggest that prepubertal exposure to PFOS may affect follicle development by disrupting estradiol production and altering Foxo1 and Gdf9 gene expression. Further studies will be important to examine the mechanisms underlying prepubertal exposure to PFOS on folliculogenesis.