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In-ovo exposed carbon black nanoparticles altered mRNA gene transcripts of antioxidants, proinflammatory and apoptotic pathways in the brain of chicken embryos

Samak, Dalia H., El-Sayed, Yasser S., Shaheen, Hazem M., El-Far, Ali H., Onoda, Atsuto, Abdel-Daim, Mohamed M., Umezawa, Masakazu·2018·Chemico-Biological Interactions
DOI 10.1016/j.cbi.2018.02.031
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Abstract

With ubiquitous applications of nanotechnology, there are increasing probabilities of exposure to manufactured nanoparticles (NPs), which might be posing emerging health concerns on the next generation. Recent data suggest that generation of reactive oxygen species may play an integral role in the carbon black nanoparticles (CBNPs)-induced oxidative injury; however, the exact molecular mechanism has not been clarified. Hence, the role of oxidative stress, inflammation and apoptosis pathways in the CBNPs-induced neuronal toxicity following in-ovo exposure of chicken embryo was elucidated. Specific pathogen-free fertilized Sasso eggs were inoculated with 4.8, 9.5 and 14 μg CBNPs/egg at the 3rd day of incubation alongside vehicle controls. In a concentration-dependent manner, CBNPs inoculation induced oxidative stress, which was ascertained by enhancement of lipid peroxides and diminishing total antioxidant capacity and glutathione levels, and catalase activity in brain tissues. mRNA transcript levels of antioxidant genes showed up-regulation of heme oxygenase-1 and superoxide dismutase-1, with marked down-regulation of glutathione S-transferase-α. Additionally, the pro-inflammatory genes; nuclear factor-κB1 was up-regulated, while interferon-γ was down-regulated. There is also a clear down-regulation in apoptotic markers caspase-8, caspase-3, cytochrome c and B-cell CLL/lymphoma 2 at the different concentrations, while caspase-2 is up-regulated only at higher concentration. Col…

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Research works printed but not linked: 62

  1. Ali, 2016, Red fluorescent carbon nanoparticle-based cell imaging probe, ACS Appl. Mater. Interfaces, 8, 9305, 10.1021/acsami.5b11318 · DOI
  2. Bhunia, 2013, Carbon nanoparticle-based fluorescent bioimaging probes, Sci. Rep., 3, 1473, 10.1038/srep01473 · DOI
  3. Jackson, 2012, Pulmonary exposure to carbon black by inhalation or instillation in pregnant mice: effects on liver DNA strand breaks in dams and offspring, Nanotoxicology, 6, 486, 10.3109/17435390.2011.587902 · DOI
  4. Kyjovska, 2015, DNA damage following pulmonary exposure by instillation to low doses of carbon black (Printex 90) nanoparticles in mice, Environ. Mol. Mutagen., 56, 41, 10.1002/em.21888 · DOI
  5. Husain, 2015, Carbon black nanoparticles induce biphasic gene expression changes associated with inflammatory responses in the lungs of C57BL/6 mice following a single intratracheal instillation, Toxicol. Appl. Pharmacol., 289, 573, 10.1016/j.taap.2015.11.003 · DOI
  6. Moller, 2005, Ultrafine particles cause cytoskeletal dysfunctions in macrophages: role of intracellular calcium, Part. Fibre Toxicol., 2, 7, 10.1186/1743-8977-2-7 · DOI
  7. Umezawa, 2018, Impact of diesel exhaust exposure on the liver of mice fed on Omega-3 polyunsaturated fatty acids-deficient diet, Food Chem. Toxicol., 111, 284, 10.1016/j.fct.2017.11.027 · DOI
  8. Shaheen, 2016, The ceramide inhibitor fumonisin B1 mitigates the pulmonary effects of low-dose diesel exhaust inhalation in mice, Ecotoxicol. Environ. Saf., 132, 390, 10.1016/j.ecoenv.2016.06.025 · DOI
  9. El-Sayed, 2015, Carbon black nanoparticle exposure during middle and late fetal development induces immune activation in male offspring mice, Toxicology, 327, 53, 10.1016/j.tox.2014.11.005 · DOI · Paper page
  10. Onoda, 2014, Effects of maternal exposure to ultrafine carbon black on brain perivascular macrophages and surrounding astrocytes in offspring mice, PLoS One, 9, 10.1371/journal.pone.0094336 · DOI · Paper page
  11. Shimizu, 2009, Maternal exposure to nanoparticulate titanium dioxide during the prenatal period alters gene expression related to brain development in the mouse, Part. Fibre Toxicol., 6, 20, 10.1186/1743-8977-6-20 · DOI
  12. 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
  13. Cela, 2014, Embryonic toxicity of nanoparticles, Cells Tissues Organs, 199, 1, 10.1159/000362163 · DOI
  14. Shah, 2011, Knowledge Synthesis Group on Determinants of Preterm LBWb. Air pollution and birth outcomes: a systematic review, Environ. Int., 37, 498, 10.1016/j.envint.2010.10.009 · DOI
  15. Yoshida, 2010, Effects of fetal exposure to carbon nanoparticles on reproductive function in male offspring, Fertil. Steril., 93, 1695, 10.1016/j.fertnstert.2009.03.094 · DOI
  16. Kyjovska, 2013, Daily sperm production: application in studies of prenatal exposure to nanoparticles in mice, Reprod. Toxicol., 36, 88, 10.1016/j.reprotox.2012.12.005 · DOI
  17. Umezawa, 2011, Maternal exposure to carbon black nanoparticle increases collagen type VIII expression in the kidney of offspring, J. Toxicol. Sci., 36, 461, 10.2131/jts.36.461 · DOI
  18. Jackson, 2011, Prenatal exposure to carbon black (printex 90): effects on sexual development and neurofunction, Basic Clin. Pharmacol. Toxicol., 109, 434, 10.1111/j.1742-7843.2011.00745.x · DOI · Paper page
  19. Shimizu, 2014, Effect of maternal exposure to carbon black nanoparticle during early gestation on the splenic phenotype of neonatal mouse, J. Toxicol. Sci., 39, 571, 10.2131/jts.39.571 · DOI
  20. 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
  21. Takeda, 2009, Nanoparticles transferred from pregnant mice to their offspring can damage the genital and cranial nerve systems, J. Health Sci., 55, 95, 10.1248/jhs.55.95 · DOI · Paper page
  22. Okada, 2013, Prenatal exposure to zinc oxide particles alters monoaminergic neurotransmitter levels in the brain of mouse offspring, J. Toxicol. Sci., 38, 363, 10.2131/jts.38.363 · DOI
  23. Donaldson, 2006, Carbon nanotubes: a review of their properties in relation to pulmonary toxicology and workplace safety, Toxicol. Sci., 92, 5, 10.1093/toxsci/kfj130 · DOI · Paper page
  24. 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
  25. Sawosz, 2014, Toxicity of pristine graphene in experiments in a chicken embryo model, Int. J. Nanomed., 9, 3913
  26. 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
  27. Wick, 2010, Barrier capacity of human placenta for nanosized materials, Environ. Health Perspect., 118, 432, 10.1289/ehp.0901200 · DOI · Paper page
  28. Prasek, 2013, Influence of nanoparticles of platinum on chicken embryo development and brain morphology, Nanoscale Res. Lett., 8, 251, 10.1186/1556-276X-8-251 · DOI
  29. Rodriguez-Fragoso, 2012, Synthesis, characterization and toxicological evaluation of maltodextrin capped cadmium sulfide nanoparticles in human cell lines and chicken embryos, J. Nanobiotechnol., 10, 47, 10.1186/1477-3155-10-47 · DOI
  30. Roman, 2013, Significant toxic role for single-walled carbon nanotubes during normal embryogenesis, Nanomedicine, 9, 945, 10.1016/j.nano.2013.03.010 · DOI
  31. Rashidi, 2009, The chick embryo: hatching a model for contemporary biomedical research, BioEssays News Rev. Mol. Cell. Dev. Biol., 31, 459, 10.1002/bies.200800168 · DOI
  32. Ribatti, 2012, Chicken chorioallantoic membrane angiogenesis model, Meth. Mol. Biol., 843, 47, 10.1007/978-1-61779-523-7_5 · DOI
  33. Henshel, 1997, The relative sensitivity of chicken embryos to yolk- or air-cell-injected 2,3,7,8-tetrachlorodibenzo-p-dioxin, Environ. Toxicol. Chem., 16, 725, 10.1002/etc.5620160417 · DOI
  34. Livak, 2001, Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method, Methods, 25, 402, 10.1006/meth.2001.1262 · DOI · Paper page
  35. Cao, 2014, Carbon black nanoparticles promote endothelial activation and lipid accumulation in macrophages independently of intracellular ROS production, PLoS One, 9, 10.1371/journal.pone.0106711 · DOI
  36. Frikke-Schmidt, 2011, Effect of vitamin C and iron chelation on diesel exhaust particle and carbon black induced oxidative damage and cell adhesion molecule expression in human endothelial cells, Toxicol Lett., 203, 181, 10.1016/j.toxlet.2011.03.011 · DOI
  37. Vesterdal, 2012, Carbon black nanoparticles and vascular dysfunction in cultured endothelial cells and artery segments, Toxicol Lett., 214, 19, 10.1016/j.toxlet.2012.07.022 · DOI
  38. Butterfield, 2002, Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal death, Neurobiol. Aging, 23, 655, 10.1016/S0197-4580(01)00340-2 · DOI
  39. Gilgun-Sherki, 2001, Oxidative stress induced-neurodegenerative diseases: the need for antioxidants that penetrate the blood brain barrier, Neuropharmacology, 40, 959, 10.1016/S0028-3908(01)00019-3 · DOI
  40. Li, 2010, Nanoparticle-induced pulmonary toxicity, Exp. Biol. Med., 235, 1025, 10.1258/ebm.2010.010021 · DOI
  41. Shvedova, 2012, Mechanisms of carbon nanotube-induced toxicity: focus on oxidative stress, Toxicol. Appl. Pharmacol., 261, 121, 10.1016/j.taap.2012.03.023 · DOI
  42. Risom, 2005, Oxidative stress-induced DNA damage by particulate air pollution, Mutat. Res., 592, 119, 10.1016/j.mrfmmm.2005.06.012 · DOI
  43. Byrne, 2008, The significance of nanoparticles in particle-induced pulmonary fibrosis, McGill J. Med. MJM Int. Forum Adv. Med. Sci. Stud., 11, 43
  44. Allen, 2000, Oxidative stress and gene regulation, Free Radic. Biol. Med., 28, 463, 10.1016/S0891-5849(99)00242-7 · DOI
  45. Manke, 2013, Mechanisms of nanoparticle-induced oxidative stress and toxicity, BioMed Res. Int., 2013, 10.1155/2013/942916 · DOI
  46. Nel, 2006, Toxic potential of materials at the nanolevel, Science, 311, 622, 10.1126/science.1114397 · DOI · Paper page
  47. Otterbein, 2003, Heme oxygenase-1: unleashing the protective properties of heme, Trends Immunol., 24, 449, 10.1016/S1471-4906(03)00181-9 · DOI
  48. Ryter, 2009, Heme oxygenase-1/carbon monoxide: from metabolism to molecular therapy, Am. J. Respir. Cell Mol. Biol., 41, 251, 10.1165/rcmb.2009-0170TR · DOI
  49. Long, 2007, Nanosize titanium dioxide stimulates reactive oxygen species in brain microglia and damages neurons in vitro, Environ. Health Perspect., 115, 1631, 10.1289/ehp.10216 · DOI
  50. Eom, 2010, p38 MAPK activation, DNA damage, cell cycle arrest and apoptosis as mechanisms of toxicity of silver nanoparticles in Jurkat T cells, Environ. Sci. Technol., 44, 8337, 10.1021/es1020668 · DOI
  51. Hsin, 2008, The apoptotic effect of nanosilver is mediated by a ROS- and JNK-dependent mechanism involving the mitochondrial pathway in NIH3T3 cells, Toxicol Lett., 179, 130, 10.1016/j.toxlet.2008.04.015 · DOI
  52. Rai, 2005, Apoptosis: a basic physiologic process in wound healing, Int. J. Low. Extrem. Wounds, 4, 138, 10.1177/1534734605280018 · DOI
  53. McIlwain, 2013, Caspase functions in cell death and disease, Cold Spring Harb. Perspect. Biol., 5, 10.1101/cshperspect.a008656 · DOI
  54. Elmore, 2007, Apoptosis: a review of programmed cell death, Toxicol. Pathol., 35, 495, 10.1080/01926230701320337 · DOI · Paper page
  55. Zamorano, 2012, A BAX/BAK and cyclophilin D-independent intrinsic apoptosis pathway, PLoS One, 7, 10.1371/journal.pone.0037782 · DOI
  56. Martinou, 2011, Mitochondria in apoptosis: Bcl-2 family members and mitochondrial dynamics, Dev. Cell, 21, 92, 10.1016/j.devcel.2011.06.017 · DOI
  57. Xia, 2006, Comparison of the abilities of ambient and manufactured nanoparticles to induce cellular toxicity according to an oxidative stress paradigm, Nano Lett., 6, 1794, 10.1021/nl061025k · DOI
  58. Lenaz, 2001, The mitochondrial production of reactive oxygen species: mechanisms and implications in human pathology, IUBMB Life, 52, 159, 10.1080/15216540152845957 · DOI · Paper page
  59. Boland, 2014, Carbon black and titanium dioxide nanoparticles induce distinct molecular mechanisms of toxicity, Wiley Interdiscip Rev. Nanomed. Nanobiotechnol., 6, 641, 10.1002/wnan.1302 · DOI
  60. Peuschel, 2012, Carbon nanoparticles induce ceramide- and lipid raft-dependent signalling in lung epithelial cells: a target for a preventive strategy against environmentally-induced lung inflammation, Part. Fibre Toxicol., 9, 48, 10.1186/1743-8977-9-48 · DOI
  61. Sydlik, 2006, Ultrafine carbon particles induce apoptosis and proliferation in rat lung epithelial cells via specific signaling pathways both using EGF-R, Am. J. Physiol. Lung Cell Mol. Physiol., 291, L725, 10.1152/ajplung.00131.2006 · DOI
  62. Periasamy, 2016, Carbon nanoparticle induced cytotoxicity in human mesenchymal stem cells through upregulation of TNF3, NFKBIA and BCL2L1 genes, Chemosphere, 144, 275, 10.1016/j.chemosphere.2015.08.018 · DOI

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Metadata

Authors
Samak, D. H., El-Sayed, Y. S., Shaheen, H. M., El-Far, A. H., Onoda, A., Abdel-Daim, M. M., & Umezawa, M.
Venue
Chemico-Biological Interactions
Publisher
Elsevier BV
Published
2018-11
Volume
295
Pages
133-139
ISSN
0009-2797
DOI
10.1016/j.cbi.2018.02.031
Cited by
20
References
1
Language
en
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CoChat. (2026). Citation check: In-ovo exposed carbon black nanoparticles altered mRNA gene transcripts of antioxidants, proinflammatory and apoptotic pathways in the brain of chicken embryos. https://app.cochat.ai/papers/10.1016/j.cbi.2018.02.031
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Samak, D. H., El-Sayed, Y. S., Shaheen, H. M., El-Far, A. H., Onoda, A., Abdel-Daim, M. M., & Umezawa, M. (2018). In-ovo exposed carbon black nanoparticles altered mRNA gene transcripts of antioxidants, proinflammatory and apoptotic pathways in the brain of chicken embryos. Chemico-Biological Interactions. https://doi.org/10.1016/j.cbi.2018.02.031