Abstract
Originalsprog | Engelsk |
---|---|
Tidsskrift | Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis |
Vol/bind | 700 |
Udgave nummer | 1-2 |
Sider (fra-til) | 39-43 |
Antal sider | 4 |
ISSN | 0027-5107 |
DOI | |
Status | Udgivet - 2010 |
Bibliografisk note
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Genotoxic potential of the perfluorinated chemicals PFOA, PFOS, PFBS, PFNA and PFHxA in human HepG2 cells. / Eriksen, Kirsten Thorup; Raaschou-Nielsen, Ole; Sørensen, Mette; Roursgaard, Martin; Loft, Steffen; Møller, Peter.
I: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, Bind 700, Nr. 1-2, 2010, s. 39-43.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Genotoxic potential of the perfluorinated chemicals PFOA, PFOS, PFBS, PFNA and PFHxA in human HepG2 cells
AU - Eriksen, Kirsten Thorup
AU - Raaschou-Nielsen, Ole
AU - Sørensen, Mette
AU - Roursgaard, Martin
AU - Loft, Steffen
AU - Møller, Peter
N1 - Keywords: Alkanesulfonic Acids; Comet Assay; DNA Damage; Environmental Monitoring; Fluorocarbons; Hep G2 Cells; Hexanoic Acids; Humans; Octanoic Acids; Oxidative Stress; Reactive Oxygen Species; Sulfonic Acids
PY - 2010
Y1 - 2010
N2 - Synthetically produced perfluorinated chemicals (PFCs) are widely used in industrial products because of their anti-wetting and surfactant properties. PFCs are suspected carcinogens and a possible mechanism of action is generation of oxidative stress. We have investigated the potential of five different PFCs to generate reactive oxygen species (ROS) and to induce oxidative DNA damage in HepG2 cells. Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) increased the intracellular ROS production by 1.52-fold (95% CI, 1.37-1.67) and 1.25-fold (95% CI, 1.10-1.40), respectively. However, the increase in ROS production was not concentration-dependent and the compounds did not generate DNA damage that could be detected by the alkaline comet assay as strand breakage and alkali-labile sites or formamidopyrimidine-DNA-glycosylase (FPG) sites. Perfluorobutane sulfonate (PFBS) and perfluorohexanoic acid (PFHxA) did not generate ROS or DNA damage. Only the exposure to perfluorononanoic acid (PFNA) caused a modest increase in DNA damage at a cytotoxic concentration level, which was detected as lactate dehydrogenase (LDH) release into the cell medium. This was not related to ROS generation. Collectively, these results indicate that PFCs induce only modest effects in terms of ROS production and DNA damage in a cell line representing the human liver.
AB - Synthetically produced perfluorinated chemicals (PFCs) are widely used in industrial products because of their anti-wetting and surfactant properties. PFCs are suspected carcinogens and a possible mechanism of action is generation of oxidative stress. We have investigated the potential of five different PFCs to generate reactive oxygen species (ROS) and to induce oxidative DNA damage in HepG2 cells. Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) increased the intracellular ROS production by 1.52-fold (95% CI, 1.37-1.67) and 1.25-fold (95% CI, 1.10-1.40), respectively. However, the increase in ROS production was not concentration-dependent and the compounds did not generate DNA damage that could be detected by the alkaline comet assay as strand breakage and alkali-labile sites or formamidopyrimidine-DNA-glycosylase (FPG) sites. Perfluorobutane sulfonate (PFBS) and perfluorohexanoic acid (PFHxA) did not generate ROS or DNA damage. Only the exposure to perfluorononanoic acid (PFNA) caused a modest increase in DNA damage at a cytotoxic concentration level, which was detected as lactate dehydrogenase (LDH) release into the cell medium. This was not related to ROS generation. Collectively, these results indicate that PFCs induce only modest effects in terms of ROS production and DNA damage in a cell line representing the human liver.
U2 - 10.1016/j.mrgentox.2010.04.024
DO - 10.1016/j.mrgentox.2010.04.024
M3 - Journal article
C2 - 20451658
VL - 700
SP - 39
EP - 43
JO - Mutation Research Letters
JF - Mutation Research Letters
SN - 0027-5107
IS - 1-2
ER -