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Pulmonary exposure to carbon black nanoparticles and vascular effects.

Vesterdal LK, Folkmann JK, Jacobsen NR, Sheykhzade M, Wallin H, Loft S, Møller P - Part Fibre Toxicol (2010)

Bottom Line: Exposure to small size particulates is regarded as a risk factor for cardiovascular diseases.Exposure 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Public Health, Section of Environmental Health, University of Copenhagen, Copenhagen, Denmark.

ABSTRACT

Background: 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. The mRNA expression of VCAM-1, ICAM-1, HO-1, and MCP-1 was examined in lung tissue.

Results: Young 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.

Conclusion: Exposure 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.

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Endothelium-dependent vasorelaxation of aorta segments from 11-13 weeks old apoE-/- mice exposed to carbon black by i.t. instillation. The response is expressed as the % relaxation of the precontraction tension produced by prostaglandin F2α. Each point on the curves represents the cumulative response at each concentration of acetylcholine (ACh). The data are expressed as the mean and SEM (see graph for n-values). * denotes a significant effect on Emax compared to the control group (P < 0.05, ANOVA with unequal variance between groups).
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Figure 1: Endothelium-dependent vasorelaxation of aorta segments from 11-13 weeks old apoE-/- mice exposed to carbon black by i.t. instillation. The response is expressed as the % relaxation of the precontraction tension produced by prostaglandin F2α. Each point on the curves represents the cumulative response at each concentration of acetylcholine (ACh). The data are expressed as the mean and SEM (see graph for n-values). * denotes a significant effect on Emax compared to the control group (P < 0.05, ANOVA with unequal variance between groups).

Mentions: 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% (95% CI: 37.0-45.5%). This was significantly lower than the Emax value for the control group which was 63.9% (95% CI: 55.5-72.3%), (Table 1, Figure 1c). No effect of CB exposure was observed in the groups of mice which received a single dose of particles 2 hours or 24 hours prior to sacrifice (Table 1, Figure 1a,b).


Pulmonary exposure to carbon black nanoparticles and vascular effects.

Vesterdal LK, Folkmann JK, Jacobsen NR, Sheykhzade M, Wallin H, Loft S, Møller P - Part Fibre Toxicol (2010)

Endothelium-dependent vasorelaxation of aorta segments from 11-13 weeks old apoE-/- mice exposed to carbon black by i.t. instillation. The response is expressed as the % relaxation of the precontraction tension produced by prostaglandin F2α. Each point on the curves represents the cumulative response at each concentration of acetylcholine (ACh). The data are expressed as the mean and SEM (see graph for n-values). * denotes a significant effect on Emax compared to the control group (P < 0.05, ANOVA with unequal variance between groups).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2991279&req=5

Figure 1: Endothelium-dependent vasorelaxation of aorta segments from 11-13 weeks old apoE-/- mice exposed to carbon black by i.t. instillation. The response is expressed as the % relaxation of the precontraction tension produced by prostaglandin F2α. Each point on the curves represents the cumulative response at each concentration of acetylcholine (ACh). The data are expressed as the mean and SEM (see graph for n-values). * denotes a significant effect on Emax compared to the control group (P < 0.05, ANOVA with unequal variance between groups).
Mentions: 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% (95% CI: 37.0-45.5%). This was significantly lower than the Emax value for the control group which was 63.9% (95% CI: 55.5-72.3%), (Table 1, Figure 1c). No effect of CB exposure was observed in the groups of mice which received a single dose of particles 2 hours or 24 hours prior to sacrifice (Table 1, Figure 1a,b).

Bottom Line: Exposure to small size particulates is regarded as a risk factor for cardiovascular diseases.Exposure 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Public Health, Section of Environmental Health, University of Copenhagen, Copenhagen, Denmark.

ABSTRACT

Background: 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. The mRNA expression of VCAM-1, ICAM-1, HO-1, and MCP-1 was examined in lung tissue.

Results: Young 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.

Conclusion: Exposure 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.

Show MeSH
Related in: MedlinePlus