Identifier: TDX:743
Authors: Fuentes de Frutos, Silvia
Abstract:
Perfluorooctane sulfonate (PFOS) is a persistent and bioaccumulative pollutant that can be released from several fluorochemicals by. The surfactant properties of this chemical have made it desirable for extensive use in industrial and commercial applications including surface protection, paper and food- package treatment, and lubricants. A number of recent studies have shown the presence of PFOS in blood samples from occupationally and non-occupationally exposed humans. Studies focused on the developmental effects of oral PFOS during pregnancy have shown dose-dependent adverse effects in rodents. Maternal and developmental toxicity were observed as reductions in maternal weight gain, reductions in fetal body weight, and delays in developmental landmarks and neuromotor maturation. Prenatal and postnatal mortality have been also reported. The toxicological profile of PFOS in adult rodents shows a significant weight loss accompanied by hepatotoxicity and reduced levels of serum cholesterol and triglycerides. However, the potential toxicity of PFOS has not been completely characterized yet. On the other hand, it has been established that gestational stress during a critical period of the embryonic development may modify gestational parameters and produce longlasting alterations in the behavior of the offspring. The presence and persistence of such adverse effects depend on factors such as the exact timing of exposure to stress of the dam and the type and intensity of stressor.It has been reported that some chemicals can alter the effects of maternal stress and, conversely, maternal stress can modify the potential adverse effects of some contaminants, in particular when they have been administered at high doses. The purpose of the present study was to evaluate whether maternal stress can modify the potential adverse effects of prenatal oral exposure to PFOS in mice.In order to assess the maternal and developmental toxicity of combined exposure to restraint stress and perfluorooctane sulfonate in mice, four groups of plug-positive female mice were orally exposed to PFOS at 0, 1.5, 3 and 6 mg/kg/day during gestation days 6-18. Four additional groups of plug-positive animals received the same PFOS doses being restrained during 30 min three times per day. Cesarean sections were performed on Day 18 of gestation and fetuses were weighed and examined for external, internal and skeletal malformations and variations. Before sacrifice of the dams, blood was collected and serum samples were prepared for thyroid hormones (total and free T3 and T4) and corticosterone analyses. In order to assess the combined effects of maternal restraint stress and (PFOS) on postnatal development and behavior of the offspring, thirty-four plug positive females were randomly divided into 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 was subjected to restraint stress (30 min per session, three sessions per day) during the same period. At 3 months of age, the offspring was evaluated for general activity in an open-field, and for learning and memory in a water maze task. After behavioral testing, serum was collected for corticosterone analyses. In order to assess the behavioral effects of PFOS on adult mice, thirty adult mice were divided into three groups. Animals were given by gavage 0, 3, and 6 mg PFOS/kg/day for four consecutive weeks. After the treatment period, mice were evaluated for several skills by testing motor and sensory function by means of a functional observation battery (FOB), general activity and exploratory behavior in an open-field, and learning and memory in a water maze task. One week after behavioral testing, serum was collected for corticosterone analyses. The results of the present study show that both PFOS and restraint stress induced maternal toxicity. PFOS-induced adverse effects on maternal and fetal toxicity in mice were observed at lower doses than those previously reported. Pups of dams exposed to 6 mg/kg of PFOS showed a reduced body weight. Moreover, PFOS exposure induced some delay in developmental landmarks and neuromotor maturation. The current results indicate that concurrent exposure to PFOS and restraint stress during pregnancy induces opposite effects on developmental parameters in the pups. These effects consist in a general delayed maturation trend induced by PFOS exposure, and a general accelerated maturation pattern induced by prenatal stress. Our results suggest interactive deleterious effects between PFOS and maternal stress on the behaviour of the offspring. Our results indicate that PFOS exposure induced only slight behavioral effects in adult male mice. In the retention test, a deleterious effect of PFOS was noted.
Repositori URV