ICAM-1 and VCAM-1 expression in rat aortic endothelial cells after single-walled carbon nanotube exposure

The expanded application of carbon nanotubes and increased annual production has recently sparked public interest concerning associated and potentially adverse exposure effects. As very little is known with regard to the toxicology and underlying mechanism of the phenomena termed "single-walled carbon nanotube (SWCNT) exposure", we conducted an in depth investigation of potential SWCNT effects on cell adhesion molecule gene expression within rat aortic endothelial cells (RAECs). RAEC exposure to SWCNT induced neutrophil adhesion to the endothelial monolayer via increased ICAM-1 and VCAM-1 expression. Due to NF-kappaB's fundamental involvement in the transcriptional regulation of cell adhesion molecules, we studied NF-kappaB/P65 activation in SWCNT treated RAECs, as well as GSH and LDH as determinants of oxidative stress, a condition that influences NF-kappaB activation. Resultant data indicates SWCNT exposure induces oxidative stress, thereby altering ICAM-1 and VCAM-1 expression. SWCNT induced nuclear NF-kB/P65 translocation can be inhibited by N-acetylcysteine, indicating elevated ICAM-1 and VCAM-1 expression is mediated by oxidative stress in RAECs, and may play important inflammatory roles in SWCNT-induced vascular endothelium damage.