CoChat
Sign Up
Cited by 96

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Exposure of pregnant mice to carbon black by intratracheal instillation: Toxicogenomic effects in dams and offspring

Jackson, Petra, Hougaard, Karin S., Vogel, Ulla, Wu, Dongmei, Casavant, Lorraine, Williams, Andrew, Wade, Mike, Yauk, Carole L., Wallin, Håkan, Halappanavar, Sabina·2012·Mutation Research/Genetic Toxicology and Environmental Mutagenesis
DOI 10.1016/j.mrgentox.2011.09.018
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.mrgentox.2011.09.018

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Figures

Image 1
CC-BY-NC-ND · From the PDF
Image 2
CC-BY-NC-ND · From the PDF
Fig. 2 Lung histology. Representative H-E and Trichrome-stained lung tissue sections from dams exposed to three different doses of CB Printex 90 (11, 54 and 268 𝛍 g/animal) 26-27 days post-exposure. (A-D) (20 × , bars 50 𝛍 m): H-E stained lung sections. Black arrows show particle deposition. (E-H) (10 × , bars 100 𝛍 m): trichrome stained lung sections showing uniform blue-stained fibrils of collagen. (I-J) (100 × , bars 10 𝛍 m): H-E stained lung sections showing inflammatory cells in CB treated samples. Solid line arrows show macrophages and dashed-line arrows indicate neutrophils.
Fig. 2 Lung histology. Representative H-E and Trichrome-stained lung tissue sections from dams exposed to three different doses of CB Printex 90 (11, 54 and 268 𝛍 g/animal) 26-27 days post-exposure. (A-D) (20 × , bars 50 𝛍 m): H-E stained lung sections. Black arrows show particle deposition. (E-H) (10 × , bars 100 𝛍 m): trichrome stained lung sections showing uniform blue-stained fibrils of collagen. (I-J) (100 × , bars 10 𝛍 m): H-E stained lung sections showing inflammatory cells in CB treated samples. Solid line arrows show macrophages and dashed-line arrows indicate neutrophils.CC-BY-NC-ND · From the PDF
Fig. 3 Tissue protein abundance. Evaluation of the abundance of several inflammatory proteins in lung tissues derived from dams exposed to three different doses of CB (11, 54 and 268 𝛍 g/animal) at the 26-27 day post-exposure time point. Numbers indicate fold changes over matched controls. Statistical significance was calculated using Student's t -test. * p -Value <0.1, ** p -value <0.01 and *** p -value< 0.001.
Fig. 3 Tissue protein abundance. Evaluation of the abundance of several inflammatory proteins in lung tissues derived from dams exposed to three different doses of CB (11, 54 and 268 𝛍 g/animal) at the 26-27 day post-exposure time point. Numbers indicate fold changes over matched controls. Statistical significance was calculated using Student's t -test. * p -Value <0.1, ** p -value <0.01 and *** p -value< 0.001.CC-BY-NC-ND · From the PDF
Fig. 4 Functional pathway analysis. Adversely affected pathways in dams ( ) male offspring ( ) and female offspring ( ). The Y -axis shows the Fisher's Exact Test p -values. The threshold line is set at 0.05.
Fig. 4 Functional pathway analysis. Adversely affected pathways in dams ( ) male offspring ( ) and female offspring ( ). The Y -axis shows the Fisher's Exact Test p -values. The threshold line is set at 0.05.CC-BY-NC-ND · From the PDF

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 67

  1. Duffin, 2007, Proinflammogenic effects of low-toxicity and metal nanoparticles in vivo and in vitro: highlighting the role of particle surface area and surface reactivity, Inhal. Toxicol., 19, 849, 10.1080/08958370701479323 · DOI · Paper page
  2. Singh, 2009, NanoGenotoxicology: the DNA damaging potential of engineered nanomaterials, Biomaterials, 30, 3891, 10.1016/j.biomaterials.2009.04.009 · DOI
  3. Schins, 2007, Genotoxicity of poorly soluble particles, Inhal. Toxicol., 19, 189, 10.1080/08958370701496202 · DOI
  4. Jacobsen, 2008, Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells, Environ. Mol. Mutagen., 49, 476, 10.1002/em.20406 · DOI
  5. Jacobsen, 2011, Mutation spectrum in FE1-MUTA(TM) mouse lung epithelial cells exposed to nanoparticulate carbon black, Environ. Mol. Mutagen., 52, 331, 10.1002/em.20629 · DOI
  6. Nurkiewicz, 2006, Systemic microvascular dysfunction and inflammation after pulmonary particulate matter exposure, Environ. Health Perspect., 114, 412, 10.1289/ehp.8413 · DOI
  7. Simeonova, 2009, Engineered nanoparticle respiratory exposure and potential risks for cardiovascular toxicity: predictive tests and biomarkers, Inhal. Toxicol., 21, 68, 10.1080/08958370902942566 · DOI
  8. Kreyling, 2002, Translocation of ultrafine insoluble iridium particles from lung epithelium to extrapulmonary organs is size dependent but very low, J. Toxicol. Environ. Health A, 65, 1513, 10.1080/00984100290071649 · DOI · Paper page
  9. Kreyling, 2009, Size dependence of the translocation of inhaled iridium and carbon nanoparticle aggregates from the lung of rats to the blood and secondary target organs, Inhal. Toxicol., 21, 55, 10.1080/08958370902942517 · DOI
  10. Oberdorster, 2002, Extrapulmonary translocation of ultrafine carbon particles following whole-body inhalation exposure of rats, J. Toxicol. Environ. Health A, 65, 1531, 10.1080/00984100290071658 · DOI · Paper page
  11. Sadauskas, 2009, Biodistribution of gold nanoparticles in mouse lung following intratracheal instillation, Chem. Cent. J., 3, 16, 10.1186/1752-153X-3-16 · DOI
  12. Sadauskas, 2007, Kupffer cells are central in the removal of nanoparticles from the organism, Part. Fibre Toxicol., 4, 10, 10.1186/1743-8977-4-10 · DOI
  13. Jacobsen, 2009, Lung inflammation and genotoxicity following pulmonary exposure to nanoparticles in ApoE−/− mice, Part. Fibre Toxicol., 6, 2, 10.1186/1743-8977-6-2 · DOI
  14. Saber, 2006, Cytokine expression in mice exposed to diesel exhaust particles by inhalation. Role of tumor necrosis factor, Part. Fibre Toxicol., 3, 4, 10.1186/1743-8977-3-4 · DOI
  15. Cho, 2010, Metal oxide nanoparticles induce unique inflammatory footprints in the lung: important implications for nanoparticle testing, Environ. Health Perspect., 118, 1699, 10.1289/ehp.1002201 · DOI
  16. Shah, 2010, Air pollution and birth outcomes: a systematic review, Environ. Int., 37, 498, 10.1016/j.envint.2010.10.009 · DOI
  17. Hougaard, 2010, Effects of prenatal exposure to surface-coated nanosized titanium dioxide (UV-Titan). A study in mice, Part. Fibre Toxicol., 7, 16, 10.1186/1743-8977-7-16 · DOI · Paper page
  18. Halappanavar, 2011, Pulmonary response to surface-coated nanotitanium dioxide particles includes induction of acute phase response genes, inflammatory cascades, and changes in microRNAs: a toxicogenomic study, Environ. Mol. Mutagen., 10.1002/em.20639 · DOI
  19. Kannan, 2007, Exposures to airborne particulate matter and adverse perinatal outcomes: a biologically plausible mechanistic framework for exploring potential, Cien. Saude Colet., 12, 1591, 10.1590/S1413-81232007000600020 · DOI
  20. Folkmann, 2009, Oxidatively damaged DNA in rats exposed by oral gavage to C60 fullerenes and single-walled carbon nanotubes, Environ. Health Perspect., 117, 703, 10.1289/ehp.11922 · DOI
  21. Jacobsen, 2007, Increased mutant frequency by carbon black, but not quartz, in the lacZ and cII transgenes of muta mouse lung epithelial cells, Environ. Mol. Mutagen., 48, 451, 10.1002/em.20300 · DOI
  22. Vesterdal, 2010, Pulmonary exposure to carbon black nanoparticles and vascular effects, Part. Fibre Toxicol., 7, 33, 10.1186/1743-8977-7-33 · DOI
  23. Wilson, 2002, Interactions between ultrafine particles and transition metals in vivo and in vitro, Toxicol. Appl. Pharmacol., 184, 172, 10.1006/taap.2002.9501 · DOI
  24. Yang, 2009, Comparative study of cytotoxicity, oxidative stress and genotoxicity induced by four typical nanomaterials: the role of particle size, shape and composition, J. Appl. Toxicol., 29, 69, 10.1002/jat.1385 · DOI
  25. Gallagher, 2003, Formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine in rat lung DNA following subchronic inhalation of carbon black, Toxicol. Appl. Pharmacol., 190, 224, 10.1016/S0041-008X(03)00187-X · DOI
  26. Brown, 2000, Increased inflammation and intracellular calcium caused by ultrafine carbon black is independent of transition metals or other soluble components, Occup. Environ. Med., 57, 685, 10.1136/oem.57.10.685 · DOI
  27. Driscoll, 1997, Cytokines and particle-induced inflammatory cell recruitment, Environ. Health Perspect., 105, 1159, 10.1289/ehp.97105s51159 · DOI
  28. Renwick, 2004, Increased inflammation and altered macrophage chemotactic responses caused by two ultrafine particle types, Occup. Environ. Med., 61, 442, 10.1136/oem.2003.008227 · DOI
  29. Sager, 2009, Surface area of particle administered versus mass in determining the pulmonary toxicity of ultrafine and fine carbon black: comparison to ultrafine titanium dioxide, Part. Fibre Toxicol., 6, 15, 10.1186/1743-8977-6-15 · DOI
  30. Saber, 2005, Tumor necrosis factor is not required for particle-induced genotoxicity and pulmonary inflammation, Arch. Toxicol., 79, 177, 10.1007/s00204-004-0613-9 · DOI
  31. Totsuka, 2009, Genotoxicity of nano/microparticles in in vitro micronuclei, in vivo comet and mutation assay systems, Part. Fibre Toxicol., 6, 23, 10.1186/1743-8977-6-23 · DOI
  32. Mohr, 2006, Pulmonary tumor types induced in Wistar rats of the so-called “19-dust study”, Exp. Toxicol. Pathol., 58, 13, 10.1016/j.etp.2006.06.001 · DOI
  33. Baan, 2006, Carcinogenicity of carbon black, titanium dioxide, and talc, Lancet Oncol., 7, 295, 10.1016/S1470-2045(06)70651-9 · DOI
  34. P. Jackson, K. Hougaard, A.M. Boisen, N.R. Jacobsen, K.A. Jensen, P. Møller, G. Brunborg, K.B. Gützkow, Pulmonary exposure to carbon black by inhalation or instillation in pregnant mice: effects on liver DNA strand breaks in dams and offspring, Nanotoxicology (2011). · DOI
  35. Jackson, 2011, An experimental protocol for maternal pulmonary exposure in developmental toxicology, Basic Clin. Pharmacol. Toxicol., 108, 202, 10.1111/j.1742-7843.2010.00644.x · DOI
  36. Kerr, 2003, Design considerations for efficient and effective microarray studies, Biometrics, 59, 822, 10.1111/j.0006-341X.2003.00096.x · DOI
  37. Kerr, 2007, Statistical design and the analysis of gene expression microarray data, Genet. Res., 89, 509, 10.1017/S0016672308009713 · DOI
  38. Benjamini, 1995, Controlling the false discovery rate: a practical and powerful approach to multiple testing, J. Roy. Stat. Soc. B (Met.), 57, 289, 10.1111/j.2517-6161.1995.tb02031.x · DOI · Paper page
  39. Huang da, 2009, Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources, Nat. Protoc., 4, 44, 10.1038/nprot.2008.211 · DOI · Paper page
  40. Jeyaseelan, 2005, Induction of CXCL5 during inflammation in the rodent lung involves activation of alveolar epithelium, Am. J. Respir. Cell Mol. Biol., 32, 531, 10.1165/rcmb.2005-0063OC · DOI
  41. Meek, 1986, Amyloid A gene family expression in different mouse tissues, J. Exp. Med., 164, 2006, 10.1084/jem.164.6.2006 · DOI
  42. Watkins, 1999, Dynamic regulation of the proinflammatory cytokine, interleukin-1beta: molecular biology for non-molecular biologists, Life Sci., 65, 449, 10.1016/S0024-3205(99)00095-8 · DOI
  43. Teeguarden, 2011, Comparative proteomics and pulmonary toxicity of instilled single-walled carbon nanotubes, crocidolite asbestos, and ultrafine carbon black in mice, Toxicol. Sci., 120, 123, 10.1093/toxsci/kfq363 · DOI
  44. Maher, 2000, Signaling by reactive oxygen species in the nervous system, Cell. Mol. Life Sci., 57, 1287, 10.1007/PL00000766 · DOI
  45. Cumming, 2004, Protein disulfide bond formation in the cytoplasm during oxidative stress, J. Biol. Chem., 279, 21749, 10.1074/jbc.M312267200 · DOI
  46. Bardwell, 1994, Building bridges: disulphide bond formation in the cell, Mol. Microbiol., 14, 199, 10.1111/j.1365-2958.1994.tb01281.x · DOI
  47. Rahman, 2006, Oxidative stress and redox regulation of lung inflammation in COPD, Eur. Respir. J., 28, 219, 10.1183/09031936.06.00053805 · DOI
  48. Szkopinska, 2005, Farnesyl diphosphate synthase; regulation of product specificity, Acta Biochim. Pol., 52, 45, 10.18388/abp.2005_3485 · DOI
  49. Li, 2010, Chronic inhibition of farnesyl pyrophosphate synthase attenuates cardiac hypertrophy and fibrosis in spontaneously hypertensive rats, Biochem. Pharmacol., 79, 399, 10.1016/j.bcp.2009.08.033 · DOI
  50. Vavricka, 2010, Purification and N-glycosylation analysis of melanoma antigen dopachrome tautomerase, Protein J., 29, 204, 10.1007/s10930-010-9241-9 · DOI
  51. Wang, 2010, Leptin in hepatocellular carcinoma, World J. Gastroenterol., 16, 5801, 10.3748/wjg.v16.i46.5801 · DOI · Paper page
  52. Bader, 2010, Dynein at the kinetochore: timing, Interactions and Functions, Semin. Cell Dev. Biol., 21, 269, 10.1016/j.semcdb.2009.12.015 · DOI
  53. Ligtenberg, 2007, Salivary agglutinin/glycoprotein-340/DMBT1: a single molecule with variable composition and with different functions in infection, inflammation and cancer, Biol. Chem., 388, 1275, 10.1515/BC.2007.158 · DOI
  54. Smith, 2000, Mammalian hexokinases and their abnormal expression in cancer, Br. J. Biomed. Sci., 57, 170
  55. Barski, 2008, The aldo-keto reductase superfamily and its role in drug metabolism and detoxification, Drug Metab. Rev., 40, 553, 10.1080/03602530802431439 · DOI
  56. Glatt, 2001, Human cytosolic sulphotransferases: genetics, characteristics, toxicological aspects, Mutat. Res., 482, 27, 10.1016/S0027-5107(01)00207-X · DOI
  57. Hodyl, 2008, Innate immune dysfunction in the neonatal rat following prenatal endotoxin exposure, J. Neuroimmunol., 204, 126, 10.1016/j.jneuroim.2008.06.041 · DOI
  58. Hodyl, 2007, Prenatal exposure to a pro-inflammatory stimulus causes delays in the development of the innate immune response to LPS in the offspring, J. Neuroimmunol., 190, 61, 10.1016/j.jneuroim.2007.07.021 · DOI
  59. Lasala, 2007, Effects of maternal exposure to LPS on the inflammatory response in the offspring, J. Neuroimmunol., 189, 95, 10.1016/j.jneuroim.2007.07.010 · DOI
  60. Surriga, 2009, Altered hepatic inflammatory response in the offspring following prenatal LPS exposure, Immunol. Lett., 123, 88, 10.1016/j.imlet.2009.02.009 · DOI
  61. Gilmore, 2004, Prenatal infection and risk for schizophrenia: IL-1beta, IL-6, and TNFalpha inhibit cortical neuron dendrite development, Neuropsychopharmacology, 29, 1221, 10.1038/sj.npp.1300446 · DOI
  62. Graciarena, 2010, Prenatal inflammation impairs adult neurogenesis and memory related behavior through persistent hippocampal TGFbeta1 downregulation, Brain Behav. Immun., 24, 1301, 10.1016/j.bbi.2010.06.005 · DOI
  63. Fedulov, 2008, Pulmonary exposure to particles during pregnancy causes increased neonatal asthma susceptibility, Am. J. Respir. Cell Mol. Biol., 38, 57, 10.1165/rcmb.2007-0124OC · DOI · Paper page
  64. Danielsen, 2010, Oxidative stress, inflammation, and DNA damage in rats after intratracheal instillation or oral exposure to ambient air and wood smoke particulate matter, Toxicol. Sci., 118, 574, 10.1093/toxsci/kfq290 · DOI
  65. Saber, 2011, Inflammatory and genotoxic effects of nanoparticles designed for inclusion in paints and lacquers, Nanotoxicology
  66. Jackson, 2011, Prenatal exposure to carbon black (Printex 90): effects on sexual development and neurofunction, Basic Clin. Pharmacol. Toxicol., 10.1111/j.1742-7843.2011.00745.x · DOI · Paper page
  67. Jacobsen, 2008, Diesel exhaust particles are mutagenic in FE1-MutaMouse lung epithelial cells, Mutat. Res., 641, 54, 10.1016/j.mrfmmm.2008.03.001 · DOI

Cited by

Sorted by citations

See all 96

Metadata

Authors
Jackson, P., Hougaard, K. S., Vogel, U., Wu, D., Casavant, L., Williams, A., Wade, M., Yauk, C. L., Wallin, H., & Halappanavar, S.
Venue
Mutation Research/Genetic Toxicology and Environmental Mutagenesis
Publisher
Elsevier BV
Published
2012-06
Volume
745
Issue
1-2
Pages
73-83
ISSN
1383-5718
DOI
10.1016/j.mrgentox.2011.09.018
Cited by
96
References
2
Language
en
Licence
Funders
  • Health Canada's Internal A-Base
  • Roskilde University
  • Danish Agency for Science, Technology and Innovation

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review