National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Environ Health Perspect. 2011 Aug;119(8):1070-6. doi: 10.1289/ehp.1002741. Epub 2011 Apr 18.
Prenatal exposure to perfluorooctanoic acid (PFOA), a ubiquitous industrial surfactant, has been reported to delay mammary gland development in female mouse offspring (F1) and the treated lactating dam (P0) after gestational treatments at 3 and 5 mg PFOA/kg/day.
We investigated the consequences of gestational and chronic PFOA exposure on F1 lactational function and subsequent development of F2 offspring.
We treated P0 dams with 0, 1, or 5 mg PFOA/kg/day on gestation days 1-17. In addition, a second group of P0 dams treated with 0 or 1 mg/kg/day during gestation and their F1 and F2 offspring received continuous PFOA exposure (5 ppb) in drinking water. Resulting adult F1 females were bred to generate F2 offspring, whose development was monitored over postnatal days (PNDs) 1-63. F1 gland function was assessed on PND10 by timed-lactation experiments. Mammary tissue was isolated from P0, F1, and F2 females throughout the study and histologically assessed for age-appropriate development.
PFOA-exposed F1 dams exhibited diminished lactational morphology, although F1 maternal behavior and F2 offspring body weights were not significantly affected by P0 treatment. In addition to reduced gland development in F1 females under all exposures, F2 females with chronic low-dose drinking-water exposures exhibited visibly slowed mammary gland differentiation from weaning onward. F2 females derived from 5 mg/kg PFOA-treated P0 dams displayed gland morphology similar to F2 chronic water exposure groups on PNDs 22-63.
Gestational PFOA exposure induced delays in mammary gland development and/or lactational differentiation across three generations. Chronic, low-dose PFOA exposure in drinking water was also sufficient to alter mammary morphological development in mice, at concentrations approximating those found in contaminated human water supplies.
全氟辛酸（PFOA）是一种普遍存在的工业表面活性剂，据报道，孕期接触 PFOA 会延迟雌性小鼠后代（F1）和经处理的哺乳期母鼠（P0）的乳腺发育，其处理方式为在妊娠第 3 天和第 5 天每天以 3 和 5 mg PFOA/kg 进行处理。
我们研究了孕期和慢性 PFOA 暴露对 F1 哺乳期功能以及随后 F2 后代发育的影响。
我们用 0、1 或 5 mg PFOA/kg/day 处理 P0 孕鼠，从妊娠第 1 天到第 17 天。此外，另一组 P0 孕鼠在妊娠期间以 0 或 1 mg/kg/day 处理，其 F1 和 F2 后代在饮用水中持续暴露于 PFOA（5 ppb）。由此产生的成年 F1 雌性与雄性交配以产生 F2 后代，监测其在产后第 1 天到第 63 天的发育情况。在产后第 10 天通过定时哺乳实验评估 F1 乳腺功能。在整个研究过程中，从 P0、F1 和 F2 雌性动物中分离出乳腺组织，并进行组织学评估以确定其与年龄相适应的发育情况。
暴露于 PFOA 的 F1 孕鼠的泌乳形态明显减少，尽管 P0 处理对 F1 母性行为和 F2 后代体重没有显著影响。除了所有暴露组中 F1 雌性的乳腺发育减少外，慢性低剂量饮用水暴露的 F2 雌性从断奶开始就表现出明显的乳腺分化缓慢。来自于经 5 mg/kg PFOA 处理的 P0 孕鼠的 F2 雌性在产后第 22 天到第 63 天期间显示出与 F2 慢性水暴露组相似的乳腺形态。
孕期 PFOA 暴露会导致三代乳腺发育和/或泌乳分化延迟。在饮用水中持续、低剂量的 PFOA 暴露也足以改变小鼠的乳腺形态发育，其浓度接近受污染的人类供水。
Zotero 插件
