Yu Wen-Guang, Liu Wei, Jin Yi-He, Liu Xiao-Hui, Wang Fa-Qi, Liu Li, Nakayama Shoji F
School of Environmental and Biological Science and Technology, Dalian University of Technology, Key Laboratory of Industrial Ecology and Environmental Engineering, Ministry of Education, Dalian 116024, China.
Environ Sci Technol. 2009 Nov 1;43(21):8416-22. doi: 10.1021/es901602d.
Perfluorooctane sulfonate (PFOS), an environmentally persistent organic pollutant, has been reported to be transferred to the developing organisms via both placenta and breast milk. A cross-foster model was used to determine whether prenatal or postnatal exposure to PFOS alone can disturb the TH homeostasis in rat pups, and if so, which kind of exposure is a major cause of TH level alteration. Pregnant rats were fed standard laboratory rodent diet containing 0 (control) or 3.2 mg PFOS/kg throughout gestation and lactation period. On the day of birth, litters born to treated and control dams were cross-fostered, resulting in the following groups: unexposed control (CC), pups exposed only prenatally (TC), only postnatally (CT) or both prenatally and postnatally (TT). Serum and liver PFOS concentrations, serum total thyroxine (T4), total triiodothyronine (T3), reverse T3 (rT3) levels, and hepatic expression of genes involved in TH transport, metabolism, and receptors were evaluated in pups at the age of postnatal days (PNDs) 0, 7, 14, 21, or 35. PFOS body burden level in pups in group CT increased, while those in group TC dropped as they aged. Neither total T3 nor rT3 in pups was affected by PFOS exposure. Gestational exposure to PFOS alone (TC) significantly (p < 0.05) decreased T4 level in pups on PNDs 21 and 35, 20.3 and 19.4% lower than the control on the same PND, respectively. Postnatal exposure to PFOS alone (CT) also induced T4 depression on PNDs 21 and 35, 28.6 and 35.9% lower than controls, respectively. No significant difference in T4 level (p > 0.05) was observed between TC and CT on these two time points. None of the selected TH related transcripts was affected by PFOS in pups on PND 0. Only transcript level of transthyretin, TH binding protein, in group TT significantly increased to 150% of the control on PND 21. The results showed that prenatal PFOS exposure and postnatal PFOS exposure induced hypothyroxinemia in rat pups to a similar extent, which suggested that in utero PFOS exposure and postnatal PFOS accumulation, especially though maternal milk, are matters of great concern.
全氟辛烷磺酸（PFOS）是一种环境持久性有机污染物，据报道可通过胎盘和母乳传递给发育中的生物体。采用交叉寄养模型来确定单独的产前或产后PFOS暴露是否会扰乱幼鼠的甲状腺激素（TH）稳态，如果是，哪种暴露是TH水平改变的主要原因。在整个妊娠期和哺乳期，给怀孕大鼠喂食含0（对照）或3.2毫克PFOS/千克的标准实验室啮齿动物饲料。在出生当天，将经处理的母鼠和对照母鼠所生的幼崽进行交叉寄养，形成以下几组：未暴露对照（CC）、仅产前暴露的幼崽（TC）、仅产后暴露的幼崽（CT）或产前和产后均暴露的幼崽（TT）。在出生后第0、7、14、21或35天评估幼鼠的血清和肝脏PFOS浓度、血清总甲状腺素（T4）、总三碘甲状腺原氨酸（T3）、反式T3（rT3）水平，以及参与TH转运、代谢和受体的基因的肝脏表达。CT组幼鼠的PFOS体内负荷水平随年龄增长而增加，而TC组幼鼠的则下降。PFOS暴露对幼鼠的总T3和rT3均无影响。仅妊娠期暴露于PFOS（TC）显著（p<0.05）降低了出生后第21天和35天幼鼠的T4水平，分别比同一时间点的对照组低20.3%和19.4%。仅产后暴露于PFOS（CT）也在出生后第21天和35天导致T4降低，分别比对照组低28.6%和35.9%。在这两个时间点，TC组和CT组的T4水平无显著差异（p>0.05）。在出生后第0天，所选的与TH相关的转录本均未受PFOS影响。仅TT组中转甲状腺素（一种TH结合蛋白）的转录水平在出生后第21天显著增加至对照组的150%。结果表明，产前PFOS暴露和产后PFOS暴露在相似程度上诱导幼鼠甲状腺素血症，这表明子宫内PFOS暴露和产后PFOS蓄积，尤其是通过母乳的蓄积，是非常值得关注的问题。
