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  • Title: Effects of perfluorooctane sulfonate on tracheal ciliary beating frequency in mice.
    Author: Matsubara E, Nakahari T, Yoshida H, Kuroiwa T, Harada KH, Inoue K, Koizumi A.
    Journal: Toxicology; 2007 Jul 17; 236(3):190-8. PubMed ID: 17544559.
    Abstract:
    Perfluorooctane sulfonate (PFOS) is one of the emerging persistent organic pollutants, ubiquitously found in the global environment, even in human serum. PFOS has been reported to perturb Ca(2+) homeostasis in Paramecium, cardiomyocytes and neurons. Since ciliary beat frequency (CBF) in the trachea is known to be increased by cytoplasmic Ca(2+) elevation, the effects of PFOS on CBF were evaluated in a slice preparation using video-enhanced contrast microscopy. PFOS increased CBF by 11% (P<0.05) at 100 microM, while it did not do so at 30 microM. At 100 microM, it increased intracellular Ca(2+) concentration ([Ca(2+)](i)) in mouse tracheal ciliary cells. In Ca(2+)-free solution, PFOS at 100 microM failed to increase CBF (0.96-fold of vehicle control). The addition of Gd(3+) (1 microM), a store-operated Ca(2+) channel blocker, did not prevent the increase in CBF (1.09-fold (P<0.01) of vehicle control). High extracellular K(+) concentration (50 mM), which causes depolarization of the plasma membrane potential and a transient increase in [Ca(2+)](i), increased CBF by 20% (P<0.05). This observation indicates involvement of voltage-dependent Ca(2+) channels (VDCCs) in stimulation of CBF. Nifedipine (30 microM), a selective VDCC blocker, antagonized the effects of high K(+) (0.92-fold of high K(+) solution) and PFOS (0.96-fold of vehicle control) on CBF. In cells from peroxisome proliferator-activated receptor alpha (PPARalpha)-null mice, PFOS still increased CBF (1.12-fold (P<0.05) of vehicle control), indicating that the actions of PFOS are not mediated via PPARalpha. These findings collectively suggest that PFOS stimulates CBF by increasing cytoplasmic Ca(2+) through VDCC.
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