Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO 2

Background: there is growing evidence that exposure to small size particulate matter increases the risk of developing cardiovascular disease.methods: we investigated plaque progression and vasodilatory function in apolipoprotein e knockout (apoe -/-) mice exposed to tio 2. apoe -/-mice were intratracheally instilled (0.5 mg/kg bodyweight) with rutile fine tio 2(ftio 2,288 nm),photocatalytic 92/8 anatase/rutile tio 2(ptio 2,12 nm),or rutile nano tio 2(ntio 2,21.6 nm) at 26 and 2 hours before measurement of vasodilatory function in aorta segments mounted in myographs. the progression of atherosclerotic plaques in aorta was assessed in mice exposed to nanosized tio 2(0.5 mg/kg bodyweight) once a week for 4 weeks. we measured mrna levels of mcp-1,mip-2,vcam-1,icam-1 and vegf in lung tissue to assess pulmonary inflammation and vascular function. tio 2-induced alterations in nitric oxide (no) production were assessed in human umbilical vein endothelial cells (huvecs).results: the exposure to ntio 2was associated with a modest increase in plaque progression in aorta,whereas there were unaltered vasodilatory function and expression levels of mcp-1,mip-2,vcam-1,icam-1 and vegf in lung tissue. the apoe -/-mice exposed to fine and photocatalytic tio 2had unaltered vasodilatory function and lung tissue inflammatory gene expression. the unaltered no-dependent vasodilatory function was supported by observations in huvecs where the no production was only increased by exposure to ntio 2.conclusion: repeated exposure to nanosized tio 2particles was associated with modest plaque progression in apoe -/-mice. there were no associations between the pulmonary tio 2exposure and inflammation or vasodilatory dysfunction. © 2011 mikkelsen et al; licensee biomed central ltd.