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

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• 作者：Lise K. Vesterdal ; Lone Mikkelsen ; Janne K. Folkmann ; Majid Sheykhzade ; Yi Cao ; Martin Roursgaard ; Steffen Loft ; Peter M?ller
• 关键词：Cell adhesion molecule ; Endothelial cell ; Nanoparticles ; Oxidative stress ; Carbon black ; Vasomotor dysfunction
• 刊名：Toxicology Letters
• 出版年：2012
• 出版时间：2 October, 2012
• 年：2012
• 卷：214
• 期：1
• 页码：19-26
• 全文大小：521 K

文摘

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 100 ¦Ìg/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 10 ¦Ìg/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 10 ¦Ìg/ml was associated with a reduced pressure-diameter relationship. Incubation with 100 ¦Ìg/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.