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.
authors.affiliation: Department of Public Health, Section of Environmental Health, University of Copenhagen, Denmark.
authors.forename: Lise K
authors.initials: LK
authors.lastname: Vesterdal
authors.forename: Lone
authors.initials: L
authors.lastname: Mikkelsen
authors.forename: Janne K
authors.initials: JK
authors.lastname: Folkmann
authors.forename: Majid
authors.initials: M
authors.lastname: Sheykhzade
authors.forename: Yi
authors.initials: Y
authors.lastname: Cao
authors.forename: Martin
authors.initials: M
authors.lastname: Roursgaard
authors.forename: Steffen
authors.initials: S
authors.lastname: Loft
authors.forename: Peter
authors.initials: P
authors.lastname: Møller
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects*; D049109:Cell Proliferation; D002470:Cell Survival / Q000187:drug effects; D042783:Endothelial Cells / Q000187:drug effects*; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D053758:Nanoparticles / Q000737:chemistry* / Q000633:toxicity*; D017382:Reactive Oxygen Species; D053260:Soot / Q000737:chemistry* / Q000633:toxicity*; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism
chemical_list: C573420:ICAM1 protein, human; D017382:Reactive Oxygen Species; D053260:Soot; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1