Rosen Mitchell B, Schmid Judith E, Das Kaberi P, Wood Carmen R, Zehr Robert D, Lau Christopher
U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Reproductive Toxicology Division, Research Triangle Park, NC, USA.
U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Reproductive Toxicology Division, Research Triangle Park, NC, USA.
Reprod Toxicol. 2009 Jun;27(3-4):278-288. doi: 10.1016/j.reprotox.2009.01.007. Epub 2009 Feb 6.
Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are environmental contaminants found in the tissues of humans and wildlife. They are activators of peroxisome proliferator-activated receptor-alpha (PPAR alpha) and exhibit hepatocarcinogenic potential in rats. PFOS and PFOA are also developmental toxicants in rodents and PFOS has been shown to induce pulmonary deficits in rat offspring. Pregnant CD-1 mice were dosed with 0, 5, or 10mg/kg PFOS from gestation days 1-17. Transcript profiling was conducted on the fetal liver and lung. Results were contrasted to data derived from a previous PFOA study. PFOS-dependent changes were primarily related to activation of PPAR alpha. No remarkable differences were found between PFOS and PFOA. Given that PPAR alpha signaling is required for neonatal mortality in PFOA-treated mice but not those exposed to PFOS, the neonatal mortality observed for PFOS may reflect functional deficits related to the physical properties of the chemical rather than to transcript alterations.
全氟辛烷磺酸（PFOS）和全氟辛酸（PFOA）是在人类和野生动物组织中发现的环境污染物。它们是过氧化物酶体增殖物激活受体α（PPARα）的激活剂，在大鼠中具有致癌潜力。PFOS和PFOA也是啮齿动物的发育毒物，并且已表明PFOS会导致大鼠后代出现肺部缺陷。在妊娠第1至17天，给怀孕的CD-1小鼠分别喂食0、5或10mg/kg的PFOS。对胎儿肝脏和肺进行转录谱分析。结果与先前一项PFOA研究的数据进行了对比。PFOS依赖性变化主要与PPARα的激活有关。未发现PFOS和PFOA之间有显著差异。鉴于PPARα信号传导是PFOA处理的小鼠新生儿死亡所必需的，但暴露于PFOS的小鼠则不然，PFOS观察到的新生儿死亡可能反映了与该化学物质物理性质相关的功能缺陷，而非转录改变。
