Neonatal death of mice treated with perfluorooctane sulfonate

Yahia, Doha; Tsukuba, Chiaki; Yoshida, Midori; Sato, Itaru; Tsuda, Shuji

doi:10.2131/jts.33.219

Cited by 43 publications

(50 citation statements)

References 15 publications

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“…We (Yahia et al, 2008) found that PFOS exposure to mice during pregnancy led to intracranial blood vessel dilatation of fetuses accompanied by severe lung collapse, which caused sudden neonatal mortality without causing still born. In spite of the fact that PFOS and PFOA are similar in causing neonatal death, the mechanism of the neonatal death may be different.…”

Section: Discussionmentioning

confidence: 87%

“…Neonatal head was examined because we found intracranial blood vessel dilatation in mice exposed to PFOS in our previous study related to neonatal death in mice exposed to PFOS (Yahia et al, 2008). Five dams (out of 10) per group were treated from GD 0 to GD 18 and left to give birth, after delivery the neonates were observed during day time for 4 days to determine the neonatal mortality.…”

Section: Postnatal Evaluationmentioning

confidence: 99%

“…In our previous study on neonatal death in mice exposed to PFOS, we found that PFOS exposure during pregnancy lead to intracranial blood vessel dilatation accompanied by severe lung collapse which caused neonatal mortality (Yahia et al, 2008). However, the neonatal death caused by PFOA has not been examined in relation to the intracranial blood vessel dilatation.…”

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confidence: 96%

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Effects of perfluorooctanoic acid (PFOA) exposure to pregnant mice on reproduction

et al. 2010

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Section: Discussionmentioning

confidence: 87%

Section: Postnatal Evaluationmentioning

confidence: 99%

mentioning

confidence: 96%

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Effects of perfluorooctanoic acid (PFOA) exposure to pregnant mice on reproduction

et al. 2010

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“…Otherwise, developmental or reproductive toxicities have been rather clearly evaluated in laboratory rodents Thibodeaux et al, 2003;Yahia et al, 2008). Timed-pregnant SD rats and CD-1 mice were given 1, 5, or 10 mg/kg PFOS by gavage daily beginning on GD 2 until term.…”

Section: Introductionmentioning

confidence: 99%

Induction of apoptosis and CYP4A1 expression in Sprague-Dawley rats exposed to low doses of perfluorooctane sulfonate

et al. 2011

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-In previous studies, perfluorooctane sulfonate (PFOS), an environmental organic compound, was reported to cause hepatotoxicity and hypolipidemia in rodents. However, the low dose toxicity of PFOS and the toxic mechanisms involved remain to be determined. To clarify the low dose toxicity and action mechanism in the target organ toxicity, Sprague-Dawley (SD) rats were orally administered with PFOS at the doses of 0, 1.25, 5, 10 mg/kg/day for 28 days. As a result, no death or abnormal symptoms were observed in all groups. The significant loss of mean body weight was observed in female rats treated with 10 mg/kg PFOS and the relative liver weight of 10 mg/kg PFOS-treated group was significantly greater compared to control. Histopathological examination revealed that fatty change was evident in the liver of male rats treated with PFOS (5 and 10 mg/kg) and hypertrophy and cellular swellings in females at the dose of 10 mg/kg, which showed different pattern of pathological lesions. In addition, we demonstrated the expression induction of hepatic caspase-3 and cytochrome P450 4A1 (CYP4A1) related with apoptosis and lipid metabolism, respectively. This study suggested that no-observed-adverseeffect level (NOAEL) of PFOS was 1.25 mg/kg in 28-day repeated toxicity study and, however, the toxic response showed gender differences. The possible toxic mechanism of PFOS was the induction of apoptosis and altering lipid metabolism which resulted in hepatotoxicity.

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“…On the other hand, the difference between PFOS-and PFOA-induced neonatal deaths was found later as follows: Yahia et al (2008) gave ICR mice 1, 10 or 20 mg/kg PFOS daily by gavage from gestational day (GD) 0 to the end of the study. Almost all fetuses at 20 mg/kg were alive on GD18 and showed normal lung structure by histopathological observation; but at parturition, all neonates were inactive and weak, showed severe lung atelectasis (almost complete collapse) and severe dilatation of intracranial blood vessel when examined histopathologically, and died within a few hours.…”

Section: Further Considerationmentioning

confidence: 99%

Differential toxicity between perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA)

Tsuda

2016

J. Toxicol. Sci.

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-Perfluoroalkyl substances (PFASs) are persistent environmental contaminants. Perfluorooctane sulfonate (PFOS) and Perfluorooctanoic acid (PFOA) are representatives of PFASs. Recently, the U.S. Environmental Protection Agency (US EPA) set the health advisory level as 70 parts per trillion for lifetime exposure to PFOS and PFOA from drinking water, based on the EPA's 2016 Health Effects Support Documents. Then, a monograph on PFOA was made available online by the International Agency for Research on Cancer, where the agency classified PFOA as "possibly carcinogenic to humans" (Group 2B). The distinction between PFOS and PFOA, however, may not be easily understood from the above documents. This paper discussed differential toxicity between PFOS and PFOA focusing on neurotoxicity, developmental toxicity and carcinogenicity, mainly based on these documents. The conclusions are as follows: Further mechanistic studies may be necessary for ultrasonic-induced PFOS-specific neurotoxicity. To support the hypothesis for PFOS-specific neonatal death that PFOS interacts directly with components of natural lung surfactant, in vivo studies to relate the physicochemical effects to lung collapse may be required. PFOA-induced DNA damage secondary to oxidative stress may develop to mutagenicity under the condition where PFOA-induced apoptosis is not sufficient to remove the damaged cells. A study to find whether PFOA induces apoptosis in normal human cells may contribute to assessment of human carcinogenicity. Studies for new targets such as hepatocyte nuclear factor 4α (HNF4α) may help clarify the underlying mechanism for PFOA-induced carcinogenicity.

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Neonatal death of mice treated with perfluorooctane sulfonate

Cited by 43 publications

References 15 publications

Effects of perfluorooctanoic acid (PFOA) exposure to pregnant mice on reproduction

Effects of perfluorooctanoic acid (PFOA) exposure to pregnant mice on reproduction

Induction of apoptosis and CYP4A1 expression in Sprague-Dawley rats exposed to low doses of perfluorooctane sulfonate

Differential toxicity between perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA)

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