Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles

Research output: Contribution to journalJournal articlepeer-review

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Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles. / Vesterdal, Lise K; Danielsen, Pernille H; Folkmann, Janne K; Jespersen, Line F; Aguilar-Pelaez, Karin; Roursgaard, Martin; Loft, Steffen; Møller, Peter.

In: Toxicology and Applied Pharmacology, Vol. 274, No. 2, 15.01.2014, p. 350-60.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Vesterdal, LK, Danielsen, PH, Folkmann, JK, Jespersen, LF, Aguilar-Pelaez, K, Roursgaard, M, Loft, S & Møller, P 2014, 'Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles', Toxicology and Applied Pharmacology, vol. 274, no. 2, pp. 350-60. https://doi.org/10.1016/j.taap.2013.10.001

APA

Vesterdal, L. K., Danielsen, P. H., Folkmann, J. K., Jespersen, L. F., Aguilar-Pelaez, K., Roursgaard, M., Loft, S., & Møller, P. (2014). Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles. Toxicology and Applied Pharmacology, 274(2), 350-60. https://doi.org/10.1016/j.taap.2013.10.001

Vancouver

Vesterdal LK, Danielsen PH, Folkmann JK, Jespersen LF, Aguilar-Pelaez K, Roursgaard M et al. Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles. Toxicology and Applied Pharmacology. 2014 Jan 15;274(2):350-60. https://doi.org/10.1016/j.taap.2013.10.001

Author

Vesterdal, Lise K ; Danielsen, Pernille H ; Folkmann, Janne K ; Jespersen, Line F ; Aguilar-Pelaez, Karin ; Roursgaard, Martin ; Loft, Steffen ; Møller, Peter. / Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles. In: Toxicology and Applied Pharmacology. 2014 ; Vol. 274, No. 2. pp. 350-60.

Bibtex

@article{f6a932b7f8144797b55328c32e5549f0,
title = "Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles",
abstract = "Exposure to particles has been suggested to generate hepatosteatosis by oxidative stress mechanisms. We investigated lipid accumulation in cultured human hepatocytes (HepG2) and rat liver after exposure to four different carbon-based particles. HepG2 cells were exposed to particles for 3h and subsequently incubated for another 18h to manifest lipid accumulation. In an animal model of metabolic syndrome we investigated the association between intake of carbon black (CB, 14nm) particles and hepatic lipid accumulation, inflammation and gene expression of Srebp-1, Fasn and Scd-1 involved in lipid synthesis. There was a concentration-dependent increase in intracellular lipid content after exposure to CB in HepG2 cells, which was only observed after co-exposure to oleic/palmitic acid. Similar results were observed in HepG2 cells after exposure to diesel exhaust particles, fullerenes C60 or pristine single-walled carbon nanotubes. All four types of particles also generated oxidatively damaged DNA, assessed as formamidopyrimidine DNA glycosylase (FPG) sensitive sites, in HepG2 cells after 3h exposure. The animal model of metabolic syndrome showed increased lipid load in the liver after one oral exposure to 6.4mg/kg of CB in lean Zucker rats. This was not associated with increased iNOS staining in the liver, indicating that the oral CB exposure was associated with hepatic steatosis rather than steatohepatitis. The lipid accumulation did not seem to be related to increased lipogenesis because there were unaltered gene expression levels in both the HepG2 cells and rat livers. Collectively, exposure to particles is associated with oxidative stress and steatosis in hepatocytes.",
author = "Vesterdal, {Lise K} and Danielsen, {Pernille H} and Folkmann, {Janne K} and Jespersen, {Line F} and Karin Aguilar-Pelaez and Martin Roursgaard and Steffen Loft and Peter M{\o}ller",
note = "{\textcopyright} 2013. Published by Elsevier Inc. All rights reserved.",
year = "2014",
month = jan,
day = "15",
doi = "10.1016/j.taap.2013.10.001",
language = "English",
volume = "274",
pages = "350--60",
journal = "Toxicology and Applied Pharmacology",
issn = "0041-008X",
publisher = "Academic Press",
number = "2",

}

RIS

TY - JOUR

T1 - Accumulation of lipids and oxidatively damaged DNA in hepatocytes exposed to particles

AU - Vesterdal, Lise K

AU - Danielsen, Pernille H

AU - Folkmann, Janne K

AU - Jespersen, Line F

AU - Aguilar-Pelaez, Karin

AU - Roursgaard, Martin

AU - Loft, Steffen

AU - Møller, Peter

N1 - © 2013. Published by Elsevier Inc. All rights reserved.

PY - 2014/1/15

Y1 - 2014/1/15

N2 - Exposure to particles has been suggested to generate hepatosteatosis by oxidative stress mechanisms. We investigated lipid accumulation in cultured human hepatocytes (HepG2) and rat liver after exposure to four different carbon-based particles. HepG2 cells were exposed to particles for 3h and subsequently incubated for another 18h to manifest lipid accumulation. In an animal model of metabolic syndrome we investigated the association between intake of carbon black (CB, 14nm) particles and hepatic lipid accumulation, inflammation and gene expression of Srebp-1, Fasn and Scd-1 involved in lipid synthesis. There was a concentration-dependent increase in intracellular lipid content after exposure to CB in HepG2 cells, which was only observed after co-exposure to oleic/palmitic acid. Similar results were observed in HepG2 cells after exposure to diesel exhaust particles, fullerenes C60 or pristine single-walled carbon nanotubes. All four types of particles also generated oxidatively damaged DNA, assessed as formamidopyrimidine DNA glycosylase (FPG) sensitive sites, in HepG2 cells after 3h exposure. The animal model of metabolic syndrome showed increased lipid load in the liver after one oral exposure to 6.4mg/kg of CB in lean Zucker rats. This was not associated with increased iNOS staining in the liver, indicating that the oral CB exposure was associated with hepatic steatosis rather than steatohepatitis. The lipid accumulation did not seem to be related to increased lipogenesis because there were unaltered gene expression levels in both the HepG2 cells and rat livers. Collectively, exposure to particles is associated with oxidative stress and steatosis in hepatocytes.

AB - Exposure to particles has been suggested to generate hepatosteatosis by oxidative stress mechanisms. We investigated lipid accumulation in cultured human hepatocytes (HepG2) and rat liver after exposure to four different carbon-based particles. HepG2 cells were exposed to particles for 3h and subsequently incubated for another 18h to manifest lipid accumulation. In an animal model of metabolic syndrome we investigated the association between intake of carbon black (CB, 14nm) particles and hepatic lipid accumulation, inflammation and gene expression of Srebp-1, Fasn and Scd-1 involved in lipid synthesis. There was a concentration-dependent increase in intracellular lipid content after exposure to CB in HepG2 cells, which was only observed after co-exposure to oleic/palmitic acid. Similar results were observed in HepG2 cells after exposure to diesel exhaust particles, fullerenes C60 or pristine single-walled carbon nanotubes. All four types of particles also generated oxidatively damaged DNA, assessed as formamidopyrimidine DNA glycosylase (FPG) sensitive sites, in HepG2 cells after 3h exposure. The animal model of metabolic syndrome showed increased lipid load in the liver after one oral exposure to 6.4mg/kg of CB in lean Zucker rats. This was not associated with increased iNOS staining in the liver, indicating that the oral CB exposure was associated with hepatic steatosis rather than steatohepatitis. The lipid accumulation did not seem to be related to increased lipogenesis because there were unaltered gene expression levels in both the HepG2 cells and rat livers. Collectively, exposure to particles is associated with oxidative stress and steatosis in hepatocytes.

U2 - 10.1016/j.taap.2013.10.001

DO - 10.1016/j.taap.2013.10.001

M3 - Journal article

C2 - 24121055

VL - 274

SP - 350

EP - 360

JO - Toxicology and Applied Pharmacology

JF - Toxicology and Applied Pharmacology

SN - 0041-008X

IS - 2

ER -

ID: 98822616