The Experts below are selected from a list of 1311 Experts worldwide ranked by ideXlab platform
Shih Houng Young - One of the best experts on this subject based on the ideXlab platform.
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Pulmonary Exposure to 1 → 3-β-Glucan Alters Adaptive Immune Responses in Rats
Inhalation Toxicology, 2020Co-Authors: Shih Houng Young, Jenny R Roberts, James M AntoniniAbstract:1 → 3-β-Glucans have been associated with increased Pulmonary inflammation in fungal-related indoor air problems. Epidemiological studies have shown a correlation between increases in T-cell proliferation and decreases in CD4+/CD8+ ratio after Exposure to fungi. The objective of the present investigation was to determine the mechanisms by which 1 → 3-β-glucans affect immune responses using an animal model. Rats received a single dose of zymosan A (2.5 mg/kg body weight) via intratracheal instillation (IT) and were euthanized on days 1, 4, 6, 8, and 10 post IT. Bronchoalveolar lavage was performed at each time point post-IT. Inflammation and lung injury were assessed by measuring neutrophil infiltration into bronchoalveolar lavage fluid (BALF) and by measuring albumin and lactate dehydrogenase levels in BALF, respectively. Alveolar macrophage activation was determined by chemiluminescence. Immune response was characterized via immunophenotyping of bronchoalveolar lavage cells and lymphocytes isolated from ...
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Increased oxidative stress with reduced responsiveness of circulating leukocytes following Pulmonary metal-rich particulate matter Exposure
The FASEB Journal, 2013Co-Authors: James M Antonini, Patti C. Zeidler-erdely, Shih Houng Young, Michael L. Kashon, Jenny R Roberts, Tracy Hulderman, Ja K Gu, Rebecca Salmen-muniz, Terence Meighan, Aaron ErdelyAbstract:Pulmonary Exposure to metal-rich particulate matter (PM) generated from welding causes localized immunosuppression. The aim of this study was to evaluate the molecular changes and responsiveness of...
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lung toxicity and biodistribution of cd se zns quantum dots with different surface functional groups after Pulmonary Exposure in rats
Particle and Fibre Toxicology, 2013Co-Authors: Jenny R Roberts, Shih Houng Young, Vincent Castranova, James M Antonini, Dale W Porter, Rebecca Chapman, James F Scabilloni, Diane Schweglerberry, Robert R MercerAbstract:Background The potential use of quantum dots (QD) in biomedical applications, as well as in other systems that take advantage of their unique physiochemical properties, has led to concern regarding their toxicity, potential systemic distribution, and biopersistence. In addition, little is known about workplace Exposure to QD in research, manufacturing, or medical settings. The goal of the present study was to assess Pulmonary toxicity, clearance, and biodistribution of QD with different functional groups in rats after Pulmonary Exposure.
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Lung toxicity and biodistribution of Cd/Se-ZnS quantum dots with different surface functional groups after Pulmonary Exposure in rats
Particle and Fibre Toxicology, 2013Co-Authors: Jenny R Roberts, Shih Houng Young, Vincent Castranova, James M Antonini, Dale W Porter, James F Scabilloni, Rebecca S Chapman, Diane Schwegler-berry, Robert R MercerAbstract:Background The potential use of quantum dots (QD) in biomedical applications, as well as in other systems that take advantage of their unique physiochemical properties, has led to concern regarding their toxicity, potential systemic distribution, and biopersistence. In addition, little is known about workplace Exposure to QD in research, manufacturing, or medical settings. The goal of the present study was to assess Pulmonary toxicity, clearance, and biodistribution of QD with different functional groups in rats after Pulmonary Exposure. Methods QD were composed of a cadmium-selenide (CdSe) core (~5nm) with a zinc sulfide (ZnS) shell functionalized with carboxyl (QD-COOH) or amine (QD-NH_2) terminal groups. Male Sprague–Dawley rats were intratracheally-instilled (IT) with saline, QD-COOH, or QD-NH_2 (12.5, 5.0, or 1.25 μg/rat). On days 0, 1, 3, 5, 7, 14, and 28 post-IT, the left lung, lung-associated lymph nodes (LALN), heart, kidneys, spleen, liver, brain, and blood were collected for metal analysis of Cd content by neutron activation to evaluate clearance and biodistribution. One right lobe was ligated and fixed for microscopy and histopathological analysis. The remaining right lobes from rats in each group were subjected to bronchoalveolar lavage (BAL) to retrieve BAL fluid and cells for analysis of injury and inflammation. Results Lung injury and inflammation was found to be dose-dependent and peaked at days 7 and 14 post-Exposure for both forms of QD, with slight variations in degree of toxicity at early and later time points. Both QD appeared to lose their fluorescent properties and destabilize after 1 week in the lung. Cd persisted up to 28 days for both forms of QD; however, clearance rate was slightly greater for QD-COOH over time. No Cd was detected in the liver, spleen, heart, brain, or blood at any time point. Cd appeared in the LALN and kidneys beginning at 1–2 weeks post-Exposure. Conclusions QD-COOH and QD-NH_2 differed in clearance rate and differed slightly in degree of toxicity at different time points; however, the overall pattern of toxicity and biodistribution was similar between the two particles. Toxicity may be dependent on the dissolution rate and bioavailability of free Cd.
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Pulmonary Exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia.
Nanotoxicology, 2011Co-Authors: Zhongxin Wu, Shih Houng Young, Teh Hsun Chen, Jared L. Cumpston, Fei Chen, Michael L. Kashon, Vincent CastranovaAbstract:AbstractThe inhalation of engineered nanoparticles stimulates the development of atherosclerosis and impairs vascular function. However, the cardiac effects of inhaled engineered nanoparticles are unknown. Here, we investigate the effects of ultrafine titanium dioxide (UFTiO2) on the heart, and we define the possible mechanisms underlying the measured effects. Pulmonary Exposure of rats to UFTiO2 increased the phosphorylation levels of p38 mitogen-activated protein kinase and cardiac troponin I, but not Akt, in the heart and substance P synthesis in nodose ganglia. Circulatory levels of pro-inflammatory cytokines, and blood cell counts and differentials were not significantly changed after Pulmonary Exposure. Separately, the incubation of cardiac myocytes isolated from naive adult rat hearts in vitro with UFTiO2 did not alter the phosphorylation status of the same cardiac proteins. In conclusion, the inhalation of UFTiO2 enhanced the phosphorylation levels of cardiac proteins. Such responses are likely in...
Robert R Mercer - One of the best experts on this subject based on the ideXlab platform.
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Effects of Pulmonary Exposure to chemically-distinct welding fumes on neuroendocrine markers of toxicity.
Journal of Toxicology and Environmental Health, 2017Co-Authors: Kristine Krajnak, Jenny R Roberts, Robert R Mercer, Krishnan Sriram, Claud Johnson, G. R. Miller, Oliver Wirth, James M AntoniniAbstract:ABSTRACTExposure to welding fumes may result in disorders of the Pulmonary, cardiovascular, and reproductive systems. Welders are also at a greater risk of developing symptoms similar to those seen in individuals with idiopathic Parkinson’s disease. In welders, there are studies that suggest that alterations in circulating prolactin concentrations may be indicative of injury to the dopamine (DA) neurons in the substantia nigra. The goal of these studies was to use an established model of welding particulate Exposure to mimic the effects of welding fume inhalation on reproductive functions. Since previous investigators suggested that changes in circulating prolactin may be an early marker of DA neuron injury, movement disorders, and reproductive dysfunction, prolactin, hypothalamic tyrosine hydroxylase (TH) levels (a marker of DA synthesis), and other measures of hypothalamic-pituitary-gonadal (HPG) function were measured after repetitive instillation of welding fume particulates generated by flux core arc...
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lung toxicity and biodistribution of cd se zns quantum dots with different surface functional groups after Pulmonary Exposure in rats
Particle and Fibre Toxicology, 2013Co-Authors: Jenny R Roberts, Shih Houng Young, Vincent Castranova, James M Antonini, Dale W Porter, Rebecca Chapman, James F Scabilloni, Diane Schweglerberry, Robert R MercerAbstract:Background The potential use of quantum dots (QD) in biomedical applications, as well as in other systems that take advantage of their unique physiochemical properties, has led to concern regarding their toxicity, potential systemic distribution, and biopersistence. In addition, little is known about workplace Exposure to QD in research, manufacturing, or medical settings. The goal of the present study was to assess Pulmonary toxicity, clearance, and biodistribution of QD with different functional groups in rats after Pulmonary Exposure.
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Lung toxicity and biodistribution of Cd/Se-ZnS quantum dots with different surface functional groups after Pulmonary Exposure in rats
Particle and Fibre Toxicology, 2013Co-Authors: Jenny R Roberts, Shih Houng Young, Vincent Castranova, James M Antonini, Dale W Porter, James F Scabilloni, Rebecca S Chapman, Diane Schwegler-berry, Robert R MercerAbstract:Background The potential use of quantum dots (QD) in biomedical applications, as well as in other systems that take advantage of their unique physiochemical properties, has led to concern regarding their toxicity, potential systemic distribution, and biopersistence. In addition, little is known about workplace Exposure to QD in research, manufacturing, or medical settings. The goal of the present study was to assess Pulmonary toxicity, clearance, and biodistribution of QD with different functional groups in rats after Pulmonary Exposure. Methods QD were composed of a cadmium-selenide (CdSe) core (~5nm) with a zinc sulfide (ZnS) shell functionalized with carboxyl (QD-COOH) or amine (QD-NH_2) terminal groups. Male Sprague–Dawley rats were intratracheally-instilled (IT) with saline, QD-COOH, or QD-NH_2 (12.5, 5.0, or 1.25 μg/rat). On days 0, 1, 3, 5, 7, 14, and 28 post-IT, the left lung, lung-associated lymph nodes (LALN), heart, kidneys, spleen, liver, brain, and blood were collected for metal analysis of Cd content by neutron activation to evaluate clearance and biodistribution. One right lobe was ligated and fixed for microscopy and histopathological analysis. The remaining right lobes from rats in each group were subjected to bronchoalveolar lavage (BAL) to retrieve BAL fluid and cells for analysis of injury and inflammation. Results Lung injury and inflammation was found to be dose-dependent and peaked at days 7 and 14 post-Exposure for both forms of QD, with slight variations in degree of toxicity at early and later time points. Both QD appeared to lose their fluorescent properties and destabilize after 1 week in the lung. Cd persisted up to 28 days for both forms of QD; however, clearance rate was slightly greater for QD-COOH over time. No Cd was detected in the liver, spleen, heart, brain, or blood at any time point. Cd appeared in the LALN and kidneys beginning at 1–2 weeks post-Exposure. Conclusions QD-COOH and QD-NH_2 differed in clearance rate and differed slightly in degree of toxicity at different time points; however, the overall pattern of toxicity and biodistribution was similar between the two particles. Toxicity may be dependent on the dissolution rate and bioavailability of free Cd.
Jenny R Roberts - One of the best experts on this subject based on the ideXlab platform.
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Pulmonary Exposure to 1 → 3-β-Glucan Alters Adaptive Immune Responses in Rats
Inhalation Toxicology, 2020Co-Authors: Shih Houng Young, Jenny R Roberts, James M AntoniniAbstract:1 → 3-β-Glucans have been associated with increased Pulmonary inflammation in fungal-related indoor air problems. Epidemiological studies have shown a correlation between increases in T-cell proliferation and decreases in CD4+/CD8+ ratio after Exposure to fungi. The objective of the present investigation was to determine the mechanisms by which 1 → 3-β-glucans affect immune responses using an animal model. Rats received a single dose of zymosan A (2.5 mg/kg body weight) via intratracheal instillation (IT) and were euthanized on days 1, 4, 6, 8, and 10 post IT. Bronchoalveolar lavage was performed at each time point post-IT. Inflammation and lung injury were assessed by measuring neutrophil infiltration into bronchoalveolar lavage fluid (BALF) and by measuring albumin and lactate dehydrogenase levels in BALF, respectively. Alveolar macrophage activation was determined by chemiluminescence. Immune response was characterized via immunophenotyping of bronchoalveolar lavage cells and lymphocytes isolated from ...
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Effects of Pulmonary Exposure to chemically-distinct welding fumes on neuroendocrine markers of toxicity.
Journal of Toxicology and Environmental Health, 2017Co-Authors: Kristine Krajnak, Jenny R Roberts, Robert R Mercer, Krishnan Sriram, Claud Johnson, G. R. Miller, Oliver Wirth, James M AntoniniAbstract:ABSTRACTExposure to welding fumes may result in disorders of the Pulmonary, cardiovascular, and reproductive systems. Welders are also at a greater risk of developing symptoms similar to those seen in individuals with idiopathic Parkinson’s disease. In welders, there are studies that suggest that alterations in circulating prolactin concentrations may be indicative of injury to the dopamine (DA) neurons in the substantia nigra. The goal of these studies was to use an established model of welding particulate Exposure to mimic the effects of welding fume inhalation on reproductive functions. Since previous investigators suggested that changes in circulating prolactin may be an early marker of DA neuron injury, movement disorders, and reproductive dysfunction, prolactin, hypothalamic tyrosine hydroxylase (TH) levels (a marker of DA synthesis), and other measures of hypothalamic-pituitary-gonadal (HPG) function were measured after repetitive instillation of welding fume particulates generated by flux core arc...
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Cardiovascular effects in rats after intratracheal instillation of metal welding particles
Inhalation Toxicology, 2015Co-Authors: Wen Zheng, Michael L. Kashon, Jenny R Roberts, James M Antonini, Vincent CastranovaAbstract:AbstractStudies have indicated that Pulmonary Exposure to welding fumes can induce a series of adverse effects in the respiratory system, including infection, bronchitis, siderosis and decreased Pulmonary function. Recent clinical and epidemiological studies have found that Pulmonary Exposure to welding fumes is also associated with a higher incidence of cardiovascular events. However, there is insufficient evidence to confirm a direct effect of welding fumes on the cardiovascular system. The present study investigated the effects of Pulmonary Exposure to welding fumes on the heart and the vascular system in rats. Two chemically distinct welding fumes generated from manual metal arc-hard surfacing (MMA-HS) and gas metal arc-mild steel (GMA-MS) welding were tested. Three groups of rats were instilled intratracheally with MMA-HS (2 mg/rat), GMA-MS (2 mg/rat) or saline as control once a week for seven weeks. On days 1 and 7 after the last treatment, basal cardiovascular function and the cardiovascular respon...
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Increased oxidative stress with reduced responsiveness of circulating leukocytes following Pulmonary metal-rich particulate matter Exposure
The FASEB Journal, 2013Co-Authors: James M Antonini, Patti C. Zeidler-erdely, Shih Houng Young, Michael L. Kashon, Jenny R Roberts, Tracy Hulderman, Ja K Gu, Rebecca Salmen-muniz, Terence Meighan, Aaron ErdelyAbstract:Pulmonary Exposure to metal-rich particulate matter (PM) generated from welding causes localized immunosuppression. The aim of this study was to evaluate the molecular changes and responsiveness of...
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lung toxicity and biodistribution of cd se zns quantum dots with different surface functional groups after Pulmonary Exposure in rats
Particle and Fibre Toxicology, 2013Co-Authors: Jenny R Roberts, Shih Houng Young, Vincent Castranova, James M Antonini, Dale W Porter, Rebecca Chapman, James F Scabilloni, Diane Schweglerberry, Robert R MercerAbstract:Background The potential use of quantum dots (QD) in biomedical applications, as well as in other systems that take advantage of their unique physiochemical properties, has led to concern regarding their toxicity, potential systemic distribution, and biopersistence. In addition, little is known about workplace Exposure to QD in research, manufacturing, or medical settings. The goal of the present study was to assess Pulmonary toxicity, clearance, and biodistribution of QD with different functional groups in rats after Pulmonary Exposure.
James M Antonini - One of the best experts on this subject based on the ideXlab platform.
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Pulmonary Exposure to 1 → 3-β-Glucan Alters Adaptive Immune Responses in Rats
Inhalation Toxicology, 2020Co-Authors: Shih Houng Young, Jenny R Roberts, James M AntoniniAbstract:1 → 3-β-Glucans have been associated with increased Pulmonary inflammation in fungal-related indoor air problems. Epidemiological studies have shown a correlation between increases in T-cell proliferation and decreases in CD4+/CD8+ ratio after Exposure to fungi. The objective of the present investigation was to determine the mechanisms by which 1 → 3-β-glucans affect immune responses using an animal model. Rats received a single dose of zymosan A (2.5 mg/kg body weight) via intratracheal instillation (IT) and were euthanized on days 1, 4, 6, 8, and 10 post IT. Bronchoalveolar lavage was performed at each time point post-IT. Inflammation and lung injury were assessed by measuring neutrophil infiltration into bronchoalveolar lavage fluid (BALF) and by measuring albumin and lactate dehydrogenase levels in BALF, respectively. Alveolar macrophage activation was determined by chemiluminescence. Immune response was characterized via immunophenotyping of bronchoalveolar lavage cells and lymphocytes isolated from ...
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Effects of Pulmonary Exposure to chemically-distinct welding fumes on neuroendocrine markers of toxicity.
Journal of Toxicology and Environmental Health, 2017Co-Authors: Kristine Krajnak, Jenny R Roberts, Robert R Mercer, Krishnan Sriram, Claud Johnson, G. R. Miller, Oliver Wirth, James M AntoniniAbstract:ABSTRACTExposure to welding fumes may result in disorders of the Pulmonary, cardiovascular, and reproductive systems. Welders are also at a greater risk of developing symptoms similar to those seen in individuals with idiopathic Parkinson’s disease. In welders, there are studies that suggest that alterations in circulating prolactin concentrations may be indicative of injury to the dopamine (DA) neurons in the substantia nigra. The goal of these studies was to use an established model of welding particulate Exposure to mimic the effects of welding fume inhalation on reproductive functions. Since previous investigators suggested that changes in circulating prolactin may be an early marker of DA neuron injury, movement disorders, and reproductive dysfunction, prolactin, hypothalamic tyrosine hydroxylase (TH) levels (a marker of DA synthesis), and other measures of hypothalamic-pituitary-gonadal (HPG) function were measured after repetitive instillation of welding fume particulates generated by flux core arc...
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Cardiovascular effects in rats after intratracheal instillation of metal welding particles
Inhalation Toxicology, 2015Co-Authors: Wen Zheng, Michael L. Kashon, Jenny R Roberts, James M Antonini, Vincent CastranovaAbstract:AbstractStudies have indicated that Pulmonary Exposure to welding fumes can induce a series of adverse effects in the respiratory system, including infection, bronchitis, siderosis and decreased Pulmonary function. Recent clinical and epidemiological studies have found that Pulmonary Exposure to welding fumes is also associated with a higher incidence of cardiovascular events. However, there is insufficient evidence to confirm a direct effect of welding fumes on the cardiovascular system. The present study investigated the effects of Pulmonary Exposure to welding fumes on the heart and the vascular system in rats. Two chemically distinct welding fumes generated from manual metal arc-hard surfacing (MMA-HS) and gas metal arc-mild steel (GMA-MS) welding were tested. Three groups of rats were instilled intratracheally with MMA-HS (2 mg/rat), GMA-MS (2 mg/rat) or saline as control once a week for seven weeks. On days 1 and 7 after the last treatment, basal cardiovascular function and the cardiovascular respon...
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Increased oxidative stress with reduced responsiveness of circulating leukocytes following Pulmonary metal-rich particulate matter Exposure
The FASEB Journal, 2013Co-Authors: James M Antonini, Patti C. Zeidler-erdely, Shih Houng Young, Michael L. Kashon, Jenny R Roberts, Tracy Hulderman, Ja K Gu, Rebecca Salmen-muniz, Terence Meighan, Aaron ErdelyAbstract:Pulmonary Exposure to metal-rich particulate matter (PM) generated from welding causes localized immunosuppression. The aim of this study was to evaluate the molecular changes and responsiveness of...
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lung toxicity and biodistribution of cd se zns quantum dots with different surface functional groups after Pulmonary Exposure in rats
Particle and Fibre Toxicology, 2013Co-Authors: Jenny R Roberts, Shih Houng Young, Vincent Castranova, James M Antonini, Dale W Porter, Rebecca Chapman, James F Scabilloni, Diane Schweglerberry, Robert R MercerAbstract:Background The potential use of quantum dots (QD) in biomedical applications, as well as in other systems that take advantage of their unique physiochemical properties, has led to concern regarding their toxicity, potential systemic distribution, and biopersistence. In addition, little is known about workplace Exposure to QD in research, manufacturing, or medical settings. The goal of the present study was to assess Pulmonary toxicity, clearance, and biodistribution of QD with different functional groups in rats after Pulmonary Exposure.
Ulla Vogel - One of the best experts on this subject based on the ideXlab platform.
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Acute phase response and inflammation following Pulmonary Exposure to low doses of zinc oxide nanoparticles in mice
Nanotoxicology, 2019Co-Authors: Niels Hadrup, Nicklas Raun Jacobsen, Hakan Wallin, Anne T. Saber, Andrew Williams, Petra Jackson, Stefan Bengtson, Feriel Rahmani, Sabina Halappanavar, Ulla VogelAbstract:AbstractInhalation of nanosized zinc oxide (ZnO) induces metal fume fever and systemic acute phase response in humans. Acute phase response activation is a cardiovascular risk factor; we investigat...
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In vivo-induced size transformation of cerium oxide nanoparticles in both lung and liver does not affect long-term hepatic accumulation following Pulmonary Exposure
PLOS ONE, 2018Co-Authors: Justyna Modrzynska, Ulla Vogel, Anne T. Saber, Alicja Mortensen, Trine Berthing, Gitte Ravn-haren, Kirsten I. Kling, Rie Romme Rasmussen, Erik Huusfeldt Larsen, Katrin LoeschnerAbstract:Recent findings show that cerium oxide (CeO2) nanoparticles may undergo in vivo-induced size transformation with the formation of smaller particles that could result in a higher translocation following Pulmonary Exposure compared to virtually insoluble particles, like titanium dioxide (TiO2). Therefore, we compared liver deposition of CeO2 and TiO2 nanoparticles of similar primary sizes 1, 28 or 180 days after intratracheal instillation of 162 μg of NPs in female C57BL/6 mice. Mice exposed to 162 μg CeO2 or TiO2 nanoparticles by intravenous injection or oral gavage were included as reference groups to assess the amount of NPs that reach the liver bypassing the lungs and the translocation of NPs from the gastrointestinal tract to the liver, respectively. Pulmonary deposited CeO2 nanoparticles were detected in the liver 28 and 180 days post-Exposure and TiO2 nanoparticles 180 days post-Exposure as determined by darkfield imaging and by the quantification of Ce and Ti mass concentration by inductively coupled plasma-mass spectrometry (ICP-MS). Ce and Ti concentrations increased over time and 180 days post-Exposure the translocation to the liver was 2.87 ± 3.37% and 1.24 ± 1.98% of the initial Pulmonary dose, respectively. Single particle ICP-MS showed that the size of CeO2 nanoparticles in both lung and liver tissue decreased over time. No nanoparticles were detected in the liver following oral gavage. Our results suggest that Pulmonary deposited CeO2 and TiO2 nanoparticles translocate to the liver with similar calculated translocation rates despite their different chemical composition and shape. The observed particle size distributions of CeO2 nanoparticles indicate in vivo processing over time both in lung and liver. The fact that no particles were detected in the liver following oral Exposure showed that direct translocation of nanoparticles from lung to the systemic circulation was the most important route of translocation for Pulmonary deposited particles.
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Pulmonary Exposure to carbonaceous nanomaterials and sperm quality.
Particle and Fibre Toxicology, 2018Co-Authors: Astrid Skovmand, Ulla Vogel, Karin Sørig Hougaard, Anna Jacobsen Lauvås, Preben Christensen, Sandra Goericke-peschAbstract:Semen quality parameters are potentially affected by nanomaterials in several ways: Inhaled nanosized particles are potent inducers of Pulmonary inflammation, leading to the release of inflammatory mediators. Small amounts of particles may translocate from the lungs into the lung capillaries, enter the systemic circulation and ultimately reach the testes. Both the inflammatory response and the particles may induce oxidative stress which can directly affect spermatogenesis. Furthermore, spermatogenesis may be indirectly affected by changes in the hormonal milieu as systemic inflammation is a potential modulator of endocrine function. The aim of this study was to investigate the effects of Pulmonary Exposure to carbonaceous nanomaterials on sperm quality parameters in an experimental mouse model. Effects on sperm quality after Pulmonary inflammation induced by carbonaceous nanomaterials were investigated by intratracheally instilling sexually mature male NMRI mice with four different carbonaceous nanomaterials dispersed in nanopure water: graphene oxide (18 μg/mouse/i.t.), Flammruss 101, Printex 90 and SRM1650b (0.1 mg/mouse/i.t. each) weekly for seven consecutive weeks. Pulmonary inflammation was determined by differential cell count in bronchoalveolar lavage fluid. Epididymal sperm concentration and motility were measured by computer-assisted sperm analysis. Epididymal sperm viability and morphological abnormalities were assessed manually using Hoechst 33,342/PI flourescent and Spermac staining, respectively. Epididymal sperm were assessed with regard to sperm DNA integrity (damage). Daily sperm production was measured in the testis, and testosterone levels were measured in blood plasma by ELISA. Neutrophil numbers in the bronchoalveolar fluid showed sustained inflammatory response in the nanoparticle-exposed groups one week after the last instillation. No significant changes in epididymal sperm parameters, daily sperm production or plasma testosterone levels were found. Despite the sustained Pulmonary inflammatory response, an eight week Exposure to graphene oxide, Flammruss 101, Printex 90 and the diesel particle SRM1650b in the present study did not appear to affect semen parameters, daily sperm production or testosterone concentration in male NMRI mice.
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Primary genotoxicity in the liver following Pulmonary Exposure to carbon black nanoparticles in mice
Particle and Fibre Toxicology, 2018Co-Authors: Justyna Modrzynska, Nicklas Raun Jacobsen, Alicja Mortensen, Ingrid Konow Weydahl, Trine Berthing, Gitte Ravn-haren, Katrin Loeschner, Anne Thoustrup Saber, Ulla VogelAbstract:Background Little is known about the mechanism underlying the genotoxicity observed in the liver following Pulmonary Exposure to carbon black (CB) nanoparticles (NPs). The genotoxicity could be caused by the presence of translocated particles or by circulating inflammatory mediators released during Pulmonary inflammation and acute-phase response. To address this, we evaluated induction of Pulmonary inflammation, Pulmonary and hepatic acute-phase response and genotoxicity following Exposure to titanium dioxide (TiO_2), cerium oxide (CeO_2) or CB NPs. Female C57BL/6 mice were exposed by intratracheal instillation, intravenous injection or oral gavage to a single dose of 162 μg NPs/mouse and terminated 1, 28 or 180 days post-Exposure alongside vehicle control. Results Liver DNA damage assessed by the Comet Assay was observed after intravenous injection and intratracheal instillation of CB NPs but not after Exposure to TiO_2 or CeO_2. Intratracheal Exposure to NPs resulted in Pulmonary inflammation in terms of increased neutrophils influx for all NPs 1 and 28 days post-Exposure. Persistent Pulmonary acute phase response was detected for all NPs at all three time points while only a transient induction of hepatic acute phase response was observed. All 3 materials were detected in the liver by enhanced darkfield microscopy up to 180 days post-Exposure. In contrast to TiO_2 and CeO_2 NPs, CB NPs generated ROS in an acellular assay. Conclusions Our results suggest that the observed hepatic DNA damage following intravenous and intratracheal dosing with CB NPs was caused by the presence of translocated, ROS-generating, particles detected in the liver rather than by the secondary effects of Pulmonary inflammation or hepatic acute phase response.
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Primary genotoxicity in the liver following Pulmonary Exposure to carbon black nanoparticles in mice
Particle and Fibre Toxicology, 2018Co-Authors: Justyna Modrzynska, Nicklas Raun Jacobsen, Anne T. Saber, Alicja Mortensen, Trine Berthing, Gitte Ravn-haren, Katrin Loeschner, Ingrid Elise Konow Weydahl, Ulla VogelAbstract:Little is known about the mechanism underlying the genotoxicity observed in the liver following Pulmonary Exposure to carbon black (CB) nanoparticles (NPs). The genotoxicity could be caused by the presence of translocated particles or by circulating inflammatory mediators released during Pulmonary inflammation and acute-phase response. To address this, we evaluated induction of Pulmonary inflammation, Pulmonary and hepatic acute-phase response and genotoxicity following Exposure to titanium dioxide (TiO2), cerium oxide (CeO2) or CB NPs. Female C57BL/6 mice were exposed by intratracheal instillation, intravenous injection or oral gavage to a single dose of 162 μg NPs/mouse and terminated 1, 28 or 180 days post-Exposure alongside vehicle control. Liver DNA damage assessed by the Comet Assay was observed after intravenous injection and intratracheal instillation of CB NPs but not after Exposure to TiO2 or CeO2. Intratracheal Exposure to NPs resulted in Pulmonary inflammation in terms of increased neutrophils influx for all NPs 1 and 28 days post-Exposure. Persistent Pulmonary acute phase response was detected for all NPs at all three time points while only a transient induction of hepatic acute phase response was observed. All 3 materials were detected in the liver by enhanced darkfield microscopy up to 180 days post-Exposure. In contrast to TiO2 and CeO2 NPs, CB NPs generated ROS in an acellular assay. Our results suggest that the observed hepatic DNA damage following intravenous and intratracheal dosing with CB NPs was caused by the presence of translocated, ROS-generating, particles detected in the liver rather than by the secondary effects of Pulmonary inflammation or hepatic acute phase response.
