胚胎期和哺乳期全氟辛烷磺酸(PFOS)暴露致大鼠学习记忆能力下降

为了探讨全氟辛烷磺酸(PFOS)的发育神经毒性，寻找PFOS发育神经毒性作用的敏感期，利用水迷宫和组织病理切片技术，研究了胚胎期和哺乳期暴露于PFOS后新生大鼠发育情况、学习记忆能力、抓力以及海马组织病理学改变。结果显示：PFOS导致仔鼠发育迟缓，睁眼期延迟。仔鼠出生后体重与对照组相比出现显著性降低。同一PFOS暴露浓度下，胚胎期暴露组体重低于哺乳期暴露组，抓力差异不显著。水迷宫实验结果显示，TT15(胚胎期和哺乳期均暴露于15 mg·L^-1 PFOS)和TC15(仅胚胎期暴露于15 mg·L^-1 PFOS)暴露组仔鼠逃避潜伏期显著高于对照组，且TC15暴露组仔鼠逃避潜伏期显著性高于CT15(仅哺乳期暴露于15 mg·L^-1 PFOS)暴露组。空间探索实验中，TT15暴露组仔鼠在目标象限的游泳时间显著性低于对照组，其他组无显著性差异。组织病理切片结果显示暴露组海马组织细胞数量减少，出现细胞凋亡现象。结果表明，PFOS造成仔鼠的发育延迟以及学习记忆能力下降的关键作用时期可能是胚胎期。

Decline of Learning and Memory Abilities in Rats Induced by Prenatal and Lactational Exposure to Perfluorooctane Sulfonate (PFOS)

The purpose of the present study is to investigate the developmental neurotoxicity of PFOS, and to identify the sensitive period of exposure. Morris Water Maze (MWM) and histopathological examinations were used to evaluate the effects of prenatal and lactational exposure to PFOS on the development of offspring. Learning and memory abilities of pups were assessed, as well as the grip of pups and pathological changes of hippocampus. The results showed that PFOS caused growth retardation, prolongation of eye opening, and reducing in birth weight of pups compared with the control group. Body weights of pups with prenatal exposure were lower than that with lactational exposure under the same concentrations of PFOS exposure. No significant change was observed in grip after PFOS exposure. MWM results showed that the escape latency of TT15 (exposed to 15 mg·L^-1 PFOS in both prenatal and lactational period) and TC15 (exposed to 15 mg·L^-1 PFOS in prenatal period) exposure groups was significantly longer than the control group. In addition, escape latency of TC15 exposure group was significantly longer than CT15 (exposed to 15 mg·L^-1 PFOS in lactational period) exposure group. Probe trial experiment suggested that the time spent in the target quadrant of pups from TT15 group was significantly shorter than those from control group, and there was no significant change in other groups. Histopathology observation indicated reduced cells and apoptosis in hippocampus. PFOS caused the developmental delay of offspring, as well as decline of learning and memory abilities, and prenatal period might be the critical stage to PFOS exposure.