Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments

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Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments. / Vesterdal, Lise K; Mikkelsen, Lone; Folkmann, Janne K; Sheykhzade, Majid; Cao, Yi; Roursgaard, Martin; Loft, Steffen; Møller, Peter.

In: Toxicology Letters, Vol. 214, No. 1, 2012, p. 19-26.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Vesterdal, LK, Mikkelsen, L, Folkmann, JK, Sheykhzade, M, Cao, Y, Roursgaard, M, Loft, S & Møller, P 2012, 'Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments', Toxicology Letters, vol. 214, no. 1, pp. 19-26. https://doi.org/10.1016/j.toxlet.2012.07.022

APA

Vesterdal, L. K., Mikkelsen, L., Folkmann, J. K., Sheykhzade, M., Cao, Y., Roursgaard, M., ... Møller, P. (2012). Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments. Toxicology Letters, 214(1), 19-26. https://doi.org/10.1016/j.toxlet.2012.07.022

Vancouver

Vesterdal LK, Mikkelsen L, Folkmann JK, Sheykhzade M, Cao Y, Roursgaard M et al. Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments. Toxicology Letters. 2012;214(1):19-26. https://doi.org/10.1016/j.toxlet.2012.07.022

Author

Vesterdal, Lise K ; Mikkelsen, Lone ; Folkmann, Janne K ; Sheykhzade, Majid ; Cao, Yi ; Roursgaard, Martin ; Loft, Steffen ; Møller, Peter. / Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments. In: Toxicology Letters. 2012 ; Vol. 214, No. 1. pp. 19-26.

Bibtex

@article{fdd0ff8e4dad40108c0df6f988e06a66,
title = "Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments",
abstract = "Exposure to small size particulates is regarded as a risk factor for cardiovascular disease. We investigated effects of exposure to nanosized carbon black (CB) in human umbilical vein endothelial cells (HUVECs) and segments of arteries from rodents. The CB exposure was associated with increased surface expression of intercellular cell adhesion molecule 1 (ICAM-1) and vascular adhesion molecule 1 (VCAM-1) in HUVECs at 100µg/ml. CB exposure was also associated with increased reactive oxygen species production and damage to the cell membranes in the form of increased lactate dehydrogenase leakage, whereas it did not alter the mitochondrial enzyme activity (WST-1) or the nitric oxide level in HUVECs. Incubation of aorta segments with 10µg/ml of CB increased the endothelial-dependent vasorelaxation, induced by acetylcholine, and shifted the endothelium-independent vasorelaxation, induced by sodium nitroprusside, towards a decreased sensitivity. In mesenteric arteries, the exposure to 10µg/ml was associated with a reduced pressure-diameter relationship. Incubation with 100µg/ml CB significantly decreased both acetylcholine and sodium nitroprusside responses as well as decreased the receptor-dependent vasoconstriction caused by phenylephrine. In conclusion, nanosized CB exposure activates endothelial cells and generates oxidative stress, which is associated with vasomotor dysfunction.",
author = "Vesterdal, {Lise K} and Lone Mikkelsen and Folkmann, {Janne K} and Majid Sheykhzade and Yi Cao and Martin Roursgaard and Steffen Loft and Peter M{\o}ller",
note = "Copyright {\circledC} 2012 Elsevier Ireland Ltd. All rights reserved.",
year = "2012",
doi = "10.1016/j.toxlet.2012.07.022",
language = "English",
volume = "214",
pages = "19--26",
journal = "Toxicology Letters",
issn = "0378-4274",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

RIS

TY - JOUR

T1 - Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments

AU - Vesterdal, Lise K

AU - Mikkelsen, Lone

AU - Folkmann, Janne K

AU - Sheykhzade, Majid

AU - Cao, Yi

AU - Roursgaard, Martin

AU - Loft, Steffen

AU - Møller, Peter

N1 - Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

PY - 2012

Y1 - 2012

N2 - Exposure to small size particulates is regarded as a risk factor for cardiovascular disease. We investigated effects of exposure to nanosized carbon black (CB) in human umbilical vein endothelial cells (HUVECs) and segments of arteries from rodents. The CB exposure was associated with increased surface expression of intercellular cell adhesion molecule 1 (ICAM-1) and vascular adhesion molecule 1 (VCAM-1) in HUVECs at 100µg/ml. CB exposure was also associated with increased reactive oxygen species production and damage to the cell membranes in the form of increased lactate dehydrogenase leakage, whereas it did not alter the mitochondrial enzyme activity (WST-1) or the nitric oxide level in HUVECs. Incubation of aorta segments with 10µg/ml of CB increased the endothelial-dependent vasorelaxation, induced by acetylcholine, and shifted the endothelium-independent vasorelaxation, induced by sodium nitroprusside, towards a decreased sensitivity. In mesenteric arteries, the exposure to 10µg/ml was associated with a reduced pressure-diameter relationship. Incubation with 100µg/ml CB significantly decreased both acetylcholine and sodium nitroprusside responses as well as decreased the receptor-dependent vasoconstriction caused by phenylephrine. In conclusion, nanosized CB exposure activates endothelial cells and generates oxidative stress, which is associated with vasomotor dysfunction.

AB - Exposure to small size particulates is regarded as a risk factor for cardiovascular disease. We investigated effects of exposure to nanosized carbon black (CB) in human umbilical vein endothelial cells (HUVECs) and segments of arteries from rodents. The CB exposure was associated with increased surface expression of intercellular cell adhesion molecule 1 (ICAM-1) and vascular adhesion molecule 1 (VCAM-1) in HUVECs at 100µg/ml. CB exposure was also associated with increased reactive oxygen species production and damage to the cell membranes in the form of increased lactate dehydrogenase leakage, whereas it did not alter the mitochondrial enzyme activity (WST-1) or the nitric oxide level in HUVECs. Incubation of aorta segments with 10µg/ml of CB increased the endothelial-dependent vasorelaxation, induced by acetylcholine, and shifted the endothelium-independent vasorelaxation, induced by sodium nitroprusside, towards a decreased sensitivity. In mesenteric arteries, the exposure to 10µg/ml was associated with a reduced pressure-diameter relationship. Incubation with 100µg/ml CB significantly decreased both acetylcholine and sodium nitroprusside responses as well as decreased the receptor-dependent vasoconstriction caused by phenylephrine. In conclusion, nanosized CB exposure activates endothelial cells and generates oxidative stress, which is associated with vasomotor dysfunction.

U2 - 10.1016/j.toxlet.2012.07.022

DO - 10.1016/j.toxlet.2012.07.022

M3 - Journal article

C2 - 22885096

VL - 214

SP - 19

EP - 26

JO - Toxicology Letters

JF - Toxicology Letters

SN - 0378-4274

IS - 1

ER -

ID: 40968355