Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments
Research output: Contribution to journal › Journal article › Research › peer-review
Standard
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 journal › Journal article › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
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