Ribes Diana, Fuentes Silvia, Torrente Margarita, Colomina M Teresa, Domingo José L
Department of Psychology and Research Center for Behavioral Assessment (CRAMC), Rovira i Virgili University, Sescelades Campus, 43007 Tarragona, Catalonia, Spain.
Toxicol Appl Pharmacol. 2010 Feb 15;243(1):13-8. doi: 10.1016/j.taap.2009.11.001. Epub 2009 Nov 10.
Although it is known that prenatal exposure to perfluorooctane sulfonate (PFOS) can cause developmental adverse effects in mammals, the disruptive effects of this compound on hormonal systems are still controversial. Information concerning the effects of PFOS on hypothalamus adrenal (HPA) axis response to stress and corticosterone levels is not currently available. On the other hand, it is well established that stress can enhance the developmental toxicity of some chemicals. In the present study, we assessed the combined effects of maternal restraint stress and PFOS on HPA axis function in the offspring of mice. Twenty plug-positive female mice were divided in two groups. Animals were given by gavage 0 and 6 mg PFOS/kg/day on gestation days 12-18. One half of the animals in each group were also subjected to restraint stress (30 min/session, 3 sessions/day) during the same period. Five plug-positive females were also included as non-manipulated controls. At 3 months of age, activity in an open-field and the stress response were evaluated in male and female mice by exposing them to 30 min of restraint stress. Male and female offspring were subsequently sacrificed and blood samples were collected to measure changes in corticosterone levels at four different moments related to stress exposure conditions: before stress exposure, immediately after 30 min of stress exposure, and recuperation levels at 60 and 90 min after stress exposure. Results indicate corticosterone levels were lower in mice prenatally exposed to restraint. In general terms, PFOS exposure decreased corticosterone levels, although this effect was only significant in females. The recuperation pattern of corticosterone was mainly affected by prenatal stress. Interactive effects between PFOS and maternal stress were sex dependent. The current results suggest that prenatal PFOS exposure induced long-lasting effects in mice.
尽管已知产前接触全氟辛烷磺酸（PFOS）会对哺乳动物的发育产生不利影响，但该化合物对激素系统的破坏作用仍存在争议。目前尚无关于PFOS对下丘脑 - 肾上腺（HPA）轴对应激反应和皮质酮水平影响的信息。另一方面，应激可增强某些化学物质的发育毒性，这一点已得到充分证实。在本研究中，我们评估了母体束缚应激和PFOS对小鼠后代HPA轴功能的联合影响。将20只确认受孕的雌性小鼠分为两组。在妊娠第12 - 18天，通过灌胃给予动物0和6 mg PFOS/kg/天。每组中的一半动物在同一时期还接受束缚应激（每次30分钟，每天3次）。还纳入了5只确认受孕的雌性小鼠作为未处理的对照。在3个月大时，通过让雄性和雌性小鼠接受30分钟的束缚应激来评估其在旷场中的活动和应激反应。随后处死雄性和雌性后代并采集血样，以测量与应激暴露条件相关的四个不同时刻的皮质酮水平变化：应激暴露前、应激暴露30分钟后立即测量，以及应激暴露后60分钟和90分钟的恢复水平。结果表明，产前暴露于束缚应激的小鼠皮质酮水平较低。总体而言，PFOS暴露会降低皮质酮水平，尽管这种影响仅在雌性中显著。皮质酮的恢复模式主要受产前应激影响。PFOS与母体应激之间的交互作用具有性别依赖性。目前的结果表明，产前PFOS暴露会在小鼠中诱导长期影响。
