(1/113) Nanomaterials induce oxidized low-density lipoprotein cellular uptake in macrophages and platelet aggregation.
BACKGROUND: Nanomaterials have numerous potential benefits for society, but the potential hazards of nanomaterials on human health are poorly understood. Nanomaterials are known to pass into the circulatory system in humans, causing vascular injuries that might play a role in the development of atherosclerosis. The present study aimed to determine the effects of chronic exposure to nanomaterials on macrophage phenotype and platelet aggregation. METHODS AND RESULTS: Cultured macrophages (RAW264.7) were treated with carbon black (CB) and water-soluble fullerene (C60(OH)24) from 7 to 50 days. Individually, CB had no significant effects on RAW264.7 cell growth, whereas C60(OH)24 alone or CB and C60(OH)24 together with oxidized low-density lipoprotein (Ox-LDL) (100 microg/ml) induced cytotoxic morphological changes, such as Ox-LDL uptake-induced foam cell-like formation and decreased cell growth, in a dose-dependent manner. C60(OH)24 induced LOX-1 protein expression, pro-matrix metalloprotease-9 protein secretion, and tissue factor mRNA expression in lipid-laden macrophages. Although CB or C60(OH)24 alone did not induce platelet aggregation, C60(OH)24 facilitated adenosine diphosphate (ADP)-induced platelet aggregation. Furthermore, C60(OH)24 acted as a competitive inhibitor of ADP receptor antagonists in ADP-mediated platelet aggregation. CONCLUSIONS: The present study confirmed novel effects of nanomaterials in macrophages and platelets. These effects suggest that exposure to nanomaterials might be a risk for atherothrombotic diseases. (+info)
(2/113) Nano-sized carbon black exposure exacerbates atherosclerosis in LDL-receptor knockout mice.
BACKGROUND: Associations between exposure to particulate matter and susceptibility to cardiovascular events have been reported. Although the underlying mechanisms are not fully understood, this association seems to be particularly exaggerated in the presence of atherothrombotic risk factors. The present study was undertaken in low-density lipoprotein receptor knockout (LDLR/KO) mice to test the hypothesis that long-term exposure to a high dose of nano-sized carbon black (CB) exacerbates atherosclerotic lesions. METHODS AND RESULTS: LDLR/KO mice were subjected to a 10-week intratracheal dispersion of CB (1 mg/week) or air under a 0% or 0.51% cholesterol (Chol) diet. Development of aortic lipid-rich lesions was detected in mice under a 0.51% Chol diet with or without CB dispersion, but not in mice fed a 0% Chol diet with or without CB. Quantification of the area stained with oil red O revealed the highest percentage in CB-treated mice on a 0.51% Chol diet among the 4 groups. One-way ANOVA indicated CB-treated mice with 0.51% Chol diet had a significantly higher percentage of positive staining than vehicle-treated mice with 0.51% Chol diet (p<0.05). CONCLUSIONS: In LDLR-deficient mice under a high Chol diet, exposure to CB resulted in acceleration of development of atherosclerosis. (+info)
(3/113) Interaction effects of ultrafine carbon black with iron and nickel on heart rate variability in spontaneously hypertensive rats.
BACKGROUND: Particulate matter (PM) has been reported to be associated with alterations in heart rate variability (HRV); however, the results are inconsistent. We propose that different components of PM cause the discrepancy. OBJECTIVE: In this study, our goal was to determine whether different types of exposure would cause different HRV effects, and to verify the interactions between co-exposing components. METHODS: Ultrafine carbon black (ufCB; 14 nm; 415 microg and 830 microg), ferric sulfate [Fe(2)(SO(4))(3); 105 microg and 210 microg], nickel sulfate (NiSO(4); 263 mug and 526 microg), and a combination of high-dose ufCB and low-dose Fe(2)(SO(4))(3) or NiSO(4) were intratracheally instilled into spontaneously hypertensive rats. Radiotelemetry data were collected in rats for 72 hr at baseline and for 72 hr the following week to determine the response to exposure. Effects of exposure on 5-min average of normal-to-normal intervals (ANN), natural logarithm-transformed standard deviation of the normal-to-normal intervals (LnSDNN), and root mean square of successive differences of adjacent normal-to-normal intervals (LnRMSSD) were analyzed using self-control experimental designs. RESULTS: Both high- and low-dose ufCB decreased ANN marginally around hour 30, with concurrent increases of LnSDNN. LnRMSSD returned to baseline levels after small initial increases. We observed minor effects after low-dose Fe and Ni instillation, whereas biphasic changes were noted after high-dose instillations. Combined exposures of ufCB and either Fe or Ni resulted in HRV trends different from values estimated from individual-component effects. CONCLUSIONS: Components in PM may induce different cardioregulatory responses, and a single component may induce different responses during different phases. Concurrent exposure to ufCB and Fe or Ni might introduce interactions on cardioregulatory effects. Also, the effect of PM may be mediated through complex interaction between different components of PM. (+info)
(4/113) Inhalation exposure to carbon black induces inflammatory response in rats.
BACKGROUND: A link between exposure to fine particulate matter and cardiovascular events has been established. Inhaled nanoparticles are thought to pass through the lungs to reach other tissues via systemic circulation and to induce cell or tissue injuries. It was recently shown that long-term exposure to intra-tracheal dispersion of nano-sized carbon black (CB) exacerbates atherosclerotic lesions in low-density lipoprotein receptor-deficient mice. Because intra-tracheal dispersion of CB may be associated with aggregate formation and may not be an ideal method for CB exposure, whole-body inhalation exposure was used in the present study, the aim of which was to examine whether exposure of rats to nano-sized CB particles by inhalation leads to translocation of these particles into the circulation, exerting direct adverse effects on extrapulmonary tissues. METHODS AND RESULTS: Sprague-Dawley rats were exposed to a high dose of CB or filtered air for 6 h/day, 5 days a week for a total of 4 weeks. Although the presence of CB was confirmed in pulmonary macrophages, electron microscopic survey did not detect CB in other tissues including liver, spleen and aorta. CB exposure raised blood pressure levels in an exposure-time dependent manner. Levels of circulating inflammatory marker proteins, including monocyte chemoattractant protein-1, interleukin-6, and C-reactive protein, were higher in the CB-treated group than in the controls. CONCLUSION: Evidence of translocation of inhaled CB was not obtained. It is likely that inhaled nano-sized CB particles form aggregations in the lung and do not exert direct adverse effects on extrapulmonary tissues. Air-pollution-mediated cardiovascular events appear to be induced by the low-grade inflammatory response to the accumulation of aggregated nano-sized particles in the lung. (+info)
(5/113) Nanoparticle carbon black driven DNA damage induces growth arrest and AP-1 and NFkappaB DNA binding in lung epithelial A549 cell line.
To assess whether nanoparticle (NP) driven DNA damage induces the expression of proinflammatory transcription factors such as NFB and AP-1 A549, lung epithelial cells were treated with Carbon Black (CB), nanoparticulate CB (NPCB), NPCB coated with BaP (BaP-NPCB) for various times ranging from 30 min to 24 h. DNA strand break was determined by the comet assay and cell cycle status was analyzed using flow cytometry. Nuclear extracts were used for WB analysis of P approximately Ser15-p53. EMSA was used to detect DNA binding. Tested NP caused single strand breaks and significantly altered cell cycle kinetics. NF-kappaB and AP-1 DNA binding were increased at early time points (2.3 and 2.6 fold at 1 hour, respectively). Effects were also found on Ser15-p53 phosphorylation. N-acetylcysteine blocked NP driven effects. In conclusion, NPCB and BaP-NPCB induce DNA damage, activating p53, proteins related to DNA repair and proinflammatory transcription factors. (+info)
(6/113) A Bayesian approach to functional-based multilevel modeling of longitudinal data: applications to environmental epidemiology.
(7/113) Fire-derived charcoal causes loss of forest humus.
(8/113) Isolation and quantitative estimation of diesel exhaust and carbon black particles ingested by lung epithelial cells and alveolar macrophages in vitro.