Effects of perfluorooctane sulfonate (PFOS) on swimming behavior and membrane potential of Paramecium caudatum
Laboratory of Veterinary Public Health, Department of Veterinary Medicine, Faculty of Agriculture, Iwate University, Morioka, Japan. The Journal of Toxicological Sciences
(Impact Factor: 1.29).
06/2008; 33(2):155-61. DOI: 10.2131/jts.33.155
Persistent perfluorinated organic compounds such as perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were distributed widely in the global. PFOS (15 microM or higher) caused backward swimming of paramecia. The Triton-extracted paramecia, where the membrane was disrupted and the externally applied chemicals are freely accessible to the ciliary apparatus, showed forward swimming up to 0.1 microM Ca2+ in the medium and backward swimming at about 0.2 microM and higher. PFOS (0.1 mM) did not change the relationship between the swimming directions and free Ca2+ concentrations. Effects of various surfactants including PFOS and PFOA on the swimming direction of paramecia were compared with the hemolysis of mouse erythrocytes as an indicator of surfactant activities. The hemolysis did not correlate with their swimming behavior. PFOS caused triphasic membrane potential changes both in the wild-type paramecia and caudatum non-reversal (CNR) mutants, the latter is defective in voltage-gated Ca2+ channels. An action potential of the wild-type specimen was induced at lower current intensity when PFOS was present in the medium. Voltage-clamp study indicated that PFOS had no effect on the depolarization-induced Ca2+ influx responsible for the action potential. The membrane potential responses obtained were similar to those obtained by the application of some bitter substances such as quinine that activate chemoreceptors of paramecia. Since the CNR specimens did not exhibit PFOS-induced backward swimming at concentrations examined, the backward swimming is attributable to the influx of Ca2+ into the cilia through voltage-gated Ca2+ channels. The Ca2+ channels are most probably activated by the depolarizing receptor potentials resulted from the PFOS-induced activation of chemoreceptors.
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- "As a consequence, contaminants can be potentially transferred along food chains and affect organisms at higher trophic levels, eventually leading to adverse effects on human health. On the other hand, an alteration in the protist component of microbial communities caused by the lethal effects of toxicants can alter the trophic chain and significantly affect the environmental balance (Yu et al., 1999; Noboru et al., 2002; Delmonte et al., 2005; Trielli et al., 2007; Kosuke et al., 2008). The main objectives of present study were to determine LC 50 and lethal concentration of monocrotophos, to investigate the cytotoxic effects under acute exposure in Paramecium caudatum and Oxytricha fallax and an attempt has been made to look into macronuclear deformities caused by monocrotophos. "
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ABSTRACT: Experiments were conducted to evaluate the toxic effects ofmonocrotophos in ciliate models Paramecium caudatum and Oxytricha fallax. In acute toxicity studies higherconcentrations of monocrotophos caused marked increase in mobility of cells exhibiting rocking movements within two mins of exposure but were decreased after 30 mins. LC50 value by mortality curve for 3 hr acute toxicity test of Oxytricha fallax and Paramecium caudatum was found 307.744 +/- 33.27 mg l(-1) and 332.284 +/- 57.52 mg l(-1) respectively. Oxytricha fallax was found sensitive than Paramecium caudatum to monocrotophos. In acute exposure cells showed deformities such as swelling, oval shaped deformity and in higher concentrations shortening of longitudinal axis with blackening of cytoplasm occurred. The length of paramecia was reduced prominently. Similarly enlargement of contractile vacuole and stress egestion of food vacuoles was also observed. The morphological studies showed the changes in shape, size, colour and width of Paramecia and Oxytricha. Frequencies of macronuclear aberrations were significant showing deformities such as rod shaped, elongation, fragmentation, diffusion and total absence of nucleus and were concentration dependent. The data provided in the present study on interaction of pesticides with nuclear structure can be of immense value because most of these pesticides have been reported to have carcinogenic, mutagenic and teratogenic properties.
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ABSTRACT: Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are widely used in industrial fields and consumer products, and are ubiquitously found in the environment and animal tissues. In the present study, their neurotoxicity was examined using rats and mice by means of neurobehavioral observation, histopathological inspection and chemical assays. PFOS and PFOA alone did not cause any neurotoxic symptoms up to their sublethal doses (PFOS: 500 mg/kg, PFOA: 1,000 mg/kg). However, tonic convulsions were caused in the PFOS-treated rats (> or = 250 mg/kg) and mice (> or = 125 mg/kg) when ultrasonic stimulus was applied to the animals. The same ultrasonic stimulus never induced convulsions in the control animals and in the animals treated with PFOA. Concentration of PFOS in the brain was considerably lower than in other tissue, but it seemed to increase gradually with time after exposure. No morphological changes were detected by histopathological examination of the brain. There were also no changes in concentrations of norepinephrine, dopamine, serotonin, glycine, 4-aminobutylic acid and glutamic acid in the brain. The present study revealed neurotoxic effects of PFOS in animals. Convulsive effect of PFOS may not be attributed to the quantitative alterations of neurotransmitters or lesions of nerve cells in the brain, although the mechanism of its neurotoxicity has not been cleared.
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