The Journal of Toxicological Sciences
Online ISSN : 1880-3989
Print ISSN : 0388-1350
ISSN-L : 0388-1350
Original Article
Ultrasonic-induced tonic convulsion in rats after subchronic exposure to perfluorooctane sulfonate (PFOS)
Kosuke KawamotoItaru SatoShuji TsudaMidori YoshidaKaori YaegashiNorimitsu SaitoWei LiuYihe Jin
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JOURNAL FREE ACCESS

2011 Volume 36 Issue 1 Pages 55-62

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Abstract

Perfluorooctane sulfonate (PFOS) is one of the persistent organic pollutants distributed widely in the global environment. We have found that a single oral administration of PFOS induced tonic convulsion in mice and rats when a brief ultrasonic stimulus was applied to the animals. The aim of this study is to examine whether the neurotoxicity is caused by subchronic dietary exposure to PFOS. Rats were treated with dietary PFOS at 0, 2, 8, 32 and 128 ppm for 13 weeks. Animals were carefully observed for pharmacotoxic signs and responses to the ultrasonic stimulus applied biweekly. PFOS increased liver weight and decreased food consumption and body weight. PFOS concentrations in the serum, brain, liver and kidney were increased almost proportional to its total dose, although the ratios of PFOS concentrations in tissues to total doses in the group treated with the highest concentration were a little lower. The ranges of relative concentrations in the brain, liver and kidney to serum concentration were 0.13 to 0.24, 2.7 to 6.3 and 0.82 to 1.6, respectively. PFOS alone did not cause any neurotoxic symptoms; however, 5 rats out of 6 showed tonic convulsion in the 6th week when ultrasonic stimulus was applied to the 128 ppm rats with the total PFOS dose of 338 mg/kg. The ultrasonic stimulus did not cause convulsion in the other groups. Histopathological examination including electron microscopic examination could not detect any abnormality in the brain. Because the acute oral dose of PFOS causing the convulsion was 250 mg/kg (Sato et al., 2009), the convulsion induced by PFOS seemed to depend on its total dose regardless of treatment schedule.

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© 2011 The Japanese Society of Toxicology
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