Abstract
BackgroundExposure to small size particulates is regarded as a risk factor for cardiovascular diseases.MethodsWe exposed young and aged apolipoprotein E knockout mice (apoE-/-) to carbon black (Printex 90, 14 nm) by intratracheal instillation, with different dosing and timing, and measured vasomotor function, progression of atherosclerotic plaques, and VCAM-1, ICAM-1, and 3-nitrotyrosine in blood vessels. The mRNA expression of VCAM-1, ICAM-1, HO-1, and MCP-1 was examined in lung tissue.ResultsYoung apoE-/- mice exposed to two consecutive 0.5 mg/kg doses of carbon black exhibited lower acetylcholine-induced vasorelaxation in aorta segments mounted in myographs, whereas single doses of 0.05-2.7 mg/kg produced no such effects. The phenylephrine-dependent vasocontraction response was shifted toward a lower responsiveness in the mice exposed once to a low dose for 24 hours. No effects were seen on the progression of atherosclerotic plaques in the aged apoE-/- mice or on the expression of VCAM-1 and ICAM-1 and the presence of 3-nitrotyrosine in the vascular tissue of either young or aged apoE-/- mice. The expression of MCP-1 mRNA was increased in the lungs of young apoE-/- mice exposed to 0.9-2.7 mg/kg carbon black for 24 hours and of aged apoE-/- mice exposed to two consecutive 0.5 mg/kg doses of carbon black seven and five weeks prior to sacrifice.ConclusionExposure to nano-sized carbon black particles is associated with modest vasomotor impairment, which is associated neither with nitrosative stress nor with any obvious increases in the expression of cell adhesion proteins on endothelial cells or in plaque progression. Evidence of pulmonary inflammation was observed, but only in animals exposed to higher doses.
Highlights
Exposure to small size particulates is regarded as a risk factor for cardiovascular diseases
In apolipoprotein E knockout mice, which are deficient in apolipoprotein E and represent a model for atherosclerosis in humans, vasomotor function is inversely correlated with plaque-size, whereas it is not affected by hypercholesterolemia [13]
Effect of carbon black on the vasomotor function in young apoE-/- mice Endothelium-dependent vasorelaxation The group of mice which received two doses of 0.5 mg/ kg CB exhibited acetylcholine-dependent vasorelaxation with an Emax value of 41.3%
Summary
Exposure to small size particulates is regarded as a risk factor for cardiovascular diseases. Methods: We exposed young and aged apolipoprotein E knockout mice (apoE-/-) to carbon black (Printex 90, 14 nm) by intratracheal instillation, with different dosing and timing, and measured vasomotor function, progression of atherosclerotic plaques, and VCAM-1, ICAM-1, and 3-nitrotyrosine in blood vessels. It has been shown that in apoE-/- mice, the acetylcholine-induced vasorelaxation was decreased and the phenylephrineinduced maximal vasocontraction was enhanced after 5 months inhalation exposure to concentrated air pollution particles [14,15]. Studies investigating the effects of exposure to particulate matter in the form of air pollution or diesel exhaust particles have shown an increased area of atherosclerotic plaques in the aorta of Watanabe heritable hyperlipidemic rabbits [26,27]
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