Genotoxic risk and oxidative DNA damage in HepG2 cells exposed to perfluorooctanoic acid

Yao, Xiaofeng; Zhong, Laifu

doi:10.1016/j.mrgentox.2005.07.010

Cited by 127 publications

(70 citation statements)

References 38 publications

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“…8-OH-dG is produced by hydroxyl radical (Gregus, 2008), which can be detected by DCFH-DA assay though its specificity is not high (Setsukinai et al, 2003). In a previous report, PFOA increased intracellular ROS in DCFH-DA assay and induced 8-OH-dG in HepG2 cells (Yao and Zhong, 2005). We detected increases in both ROS in the DCFH-DA assay and DNA damages in the comet assay; however we detect neither the DNA strand brakes nor increase in 8-OH-dG level.…”

Section: Discussionmentioning

confidence: 99%

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Perfluorooctanoic acid (PFOA) but not perfluorooctane sulfonate (PFOS) showed DNA damage in comet assay on Paramecium caudatum

et al. 2010

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Section: Discussionmentioning

confidence: 99%

“…On the other hand, Yao and Zhong (2005) reported that PFOA increased intracellular reactive oxygen species (ROS), 8-hydroxydeoxyguanosine (8-OH-dG) and induced DNA strand breaks and micronuclei in HepG2 cells. Takagi et al (1991) reported PFOA-induced 8-OHdG in rat liver.…”

Section: Introductionmentioning

confidence: 99%

Perfluorooctanoic acid (PFOA) but not perfluorooctane sulfonate (PFOS) showed DNA damage in comet assay on Paramecium caudatum

et al. 2010

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“…However, only two studies reported by Yao and Zhong (2005) and Zhao et al (2011) showed PFOA-induced mutation. In general, activation of PPAR α suppresses apoptosis as follows: Roberts et al (1998) indicated that activation of rat liver PPARα provides a survival signal for hepatocytes, preventing their death in response to apoptotic stimuli.…”

Section: Further Considerationmentioning

confidence: 97%

“…The cited report showed PFOA-induced positive results in MN assay, in addition to increased levels of 8-OH-dG, ROS, and DNA strand breaks in cultured human hepatoma HepG2 cells (Yao and Zhong, 2005). The monograph concluded as follows: PFOA is not DNA-reactive, with negative results in an overwhelming number of assays for direct genotoxicity.…”

Section: Carcinogenicity Hesd and Iarc Descriptionsmentioning

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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“…However, in human HepG2 cells this compound exerted genotoxic effects as a consequence of oxidative stress (Yao and Zhong, 2005). In rodents dietary intake of PFOA induced tumors of the testicles, liver, and pancreas (Biegel et al, 2001;Sibinski, 1987).…”

Section:  Tumor Inductionmentioning

confidence: 99%

Per- and polyfluorinated substances in the Nordic Countries

Posner

Roos

Poulsen

et al. 2013

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Genotoxic risk and oxidative DNA damage in HepG2 cells exposed to perfluorooctanoic acid

Cited by 127 publications

References 38 publications

Perfluorooctanoic acid (PFOA) but not perfluorooctane sulfonate (PFOS) showed DNA damage in comet assay on Paramecium caudatum

Perfluorooctanoic acid (PFOA) but not perfluorooctane sulfonate (PFOS) showed DNA damage in comet assay on Paramecium caudatum

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

Per- and polyfluorinated substances in the Nordic Countries

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