Mixing of perfluorooctanesulfonic acid (PFOS) potassium salt with dipalmitoyl phosphatidylcholine (DPPC)

Department of Chemical and Materials Engineering, University of Kentucky, Lexington, Kentucky, United States
Colloids and surfaces B: Biointerfaces (Impact Factor: 4.15). 09/2006; 51(1):25-9. DOI: 10.1016/j.colsurfb.2006.05.013
Source: PubMed


Perfluorooctane-1-sulfonic acid (PFOS) is emerging as an important persistent environmental pollutant. To gain insight into the interaction of PFOS with biological systems, the mixing behavior of dipalmitoylphosphatidylcholine (DPPC) with PFOS was studied using differential scanning calorimetry (DSC) and fluorescence anisotropy measurements. In the DSC experiments the onset temperature of the DPPC pretransition (Tp) decreased with increasing PFOS concentration, disappearing at XDPPC < or = 0.97. The main DPPC phase transition temperature showed a depression and peak broadening with increasing mole fraction of PFOS in both the DSC and the fluorescence anisotropy studies. From the melting point depression in the fluorescence anisotropy studies, which was observed at a concentration as low as 10 mg/L, an apparent partition coefficient of K = 5.7 x 10(4) (mole fraction basis) was calculated. These results suggest that PFOS has a high tendency to partition into lipid bilayers. These direct PFOS-DPPC interactions are one possible mechanism by which PFOS may contribute to adverse effects, for example neonatal mortality, in laboratory studies and possibly in humans.

Download full-text


Available from: Hans-Joachim Lehmler
  • Source
    • "Dipalmitoylphosphatidylcholine (DPPC) is one of the main phospholipid components in surfactant. Lehmler et al. [51] used DPPC model bilayer membranes to evaluate the effects of PFOS on membrane stability using differential scanning calorimetry and fluorescence anisotropy measurements. PFOS was found to partition into and affect the model membranes, changing membrane fluidity at concentrations as low as 10 mg/L. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are members of a family of perfluorinated compounds. Both are environmentally persistent and found in the serum of wildlife and humans. PFOS and PFOA are developmentally toxic in laboratory rodents. Exposure to these chemicals in utero delays development and reduces postnatal survival and growth. Exposure to PFOS on the last 4 days of gestation in the rat is sufficient to reduce neonatal survival. PFOS and PFOA are weak agonists of peroxisome proliferator activated receptor-alpha (PPAR alpha). The reduced postnatal survival of neonatal mice exposed to PFOA was recently shown to depend on expression of PPAR alpha. This study used PPAR alpha knockout (KO) and 129S1/SvlmJ wild type (WT) mice to determine if PPAR alpha expression is required for the developmental toxicity of PFOS. After mating overnight, the next day was designated gestation day (GD) 0. WT females were weighed and dosed orally from GD15 to 18 with 0.5% Tween-20, 4.5, 6.5, 8.5, or 10.5mg PFOS/kg/day. KO females were dosed with 0.5% Tween-20, 8.5 or 10.5mg PFOS/kg/day. Dams and pups were observed daily and pups were weighed on postnatal day (PND) 1 and PND15. Eye opening was recorded from PND12 to 15. Dams and pups were killed on PND15, body and liver weights recorded, and serum collected. PFOS did not affect maternal weight gain or body or liver weights of the dams on PND15. Neonatal survival (PND1-15) was significantly reduced by PFOS in both WT and KO litters at all doses. WT and KO pup birth weight and weight gain from PND1 to 15 were not significantly affected by PFOS exposure. Relative liver weight of WT and KO pups was significantly increased by the 10.5mg/kg dose. Eye opening of PFOS-exposed pups was slightly delayed in WT and KO on PND13 or 14, respectively. Because results in WT and KO were comparable, it is concluded that PFOS-induced neonatal lethality and delayed eye opening are not dependent on activation of PPAR alpha.
    Full-text · Article · Jun 2008 · Reproductive Toxicology
  • Source
    • "n . The rescuing agents also failed to mitigate the extent of PFOS - induced neonatal mortality . These investigators surmised that the labored breathing and subsequent mortality observed in the PFOS - exposed newborns might not be related to immaturity of the lung per se . This contention , in fact , is consistent with recent findings reported by Lehmler et al . ( 2006 ) . These researchers examined the mixing behavior of dipalmitoylphos - phatidylcholine ( DPPC ) , a major component of pulmonary surfactant , with PFOS by differential scanning calorimetry and fluorescence anisotropy measurements . They noted that PFOS had a high tendency to partition into lipid bilayers . Such PFOS – DPPC physical int"
    [Show abstract] [Hide abstract]
    ABSTRACT: In recent years, human and wildlife monitoring studies have identified perfluoroalkyl acids (PFAA) worldwide. This has led to efforts to better understand the hazards that may be inherent in these compounds, as well as the global distribution of the PFAAs. Much attention has focused on understanding the toxicology of the two most widely known PFAAs, perfluorooctanoic acid, and perfluorooctane sulfate. More recently, research was extended to other PFAAs. There has been substantial progress in understanding additional aspects of the toxicology of these compounds, particularly related to the developmental toxicity, immunotoxicity, hepatotoxicity, and the potential modes of action. This review provides an overview of the recent advances in the toxicology and mode of action for PFAAs, and of the monitoring data now available for the environment, wildlife, and humans. Several avenues of research are proposed that would further our understanding of this class of compounds.
    Full-text · Article · Nov 2007 · Toxicological Sciences
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Perfluorooctanesulfonic acid (PFOS) is a persistent environmental pollutant that may cause adverse effects by inhibiting pulmonary surfactant. To gain further insights in this potential mechanism of toxicity, we investigated the interaction of PFOS potassium salt with dipalmitoylphosphatidylcholine (DPPC) - the major component of pulmonary surfactant - using steady-state fluorescence anisotropy spectroscopy and DSC (differential scanning calorimetry). In addition, we investigated the interactions of two structurally related compounds, perfluorooctanoic acid (PFOA) and octanesulfonic acid (OS) potassium salt, with DPPC. In the fluorescence experiments a linear depression of the main phase transition temperature of DPPC (T(m)) and an increased peak width was observed with increasing concentration of all three compounds, both using 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene p-toluenesulfonate (TMA-DPH) as fluorescent probes. PFOS caused an effect on T(m) and peak width at much lower concentrations because of its increased tendency to partition onto DPPC bilayers, i.e., the partition coefficients decrease in the K(PFOS)>K(PFOA)>K(OS). Similar to the fluorescence anisotropy measurements, all three compounds caused a linear depression in the onset of the main phase transition temperature and a significant peak broadening in the DSC experiments, with PFOS having the most pronounced effect of the peak width. The effect of PFOS and other fluorinated surfactants on DPPC in both mono- and bilayers may be one mechanism by which these compounds cause adverse biological effects.
    Full-text · Article · May 2007 · Biochimica et Biophysica Acta
Show more