Titán-dioxid-nanopálcikák tüdore kifejtett hatásának állatkísérletes vizsgálata szubakut patkánymodellben

Tamara Horváth, A. Papp, Mónika Kiricsi, Nóra Igaz, Vivien Trenka, Gábor Kozma, L. Tiszlavicz, Zsolt Rázga, Tünde Vezér

Research output: Article

Abstract

Introduction: The development of nanotechnology increases the risk of occupational and population-level exposure to nanoparticles nowadays. However, scientifically based knowledge relating to the toxicity of heavy metal nanoparticles and potential health damage is insufficient. Aim: Investigation of lung tissue damage induced by titanium dioxide (TiO2) nanorods in subacute intratracheal instillation by morphological, chemical and biochemical methods in rat model. Method: General toxicity (changes of body and organ weights), local acute and chronic cellular toxicity (in alveolar spaces and epithelium, in hilar lymph nodes) and oxidative stress were examined using light and electron microscopy, and biochemical methods (reactive oxygen species, lipid peroxidation, expression of pro-inflammatory cytokines). Results: No dose- and time-dependent alteration was found in the body weight of the treated groups; but the mass and Ti content of lungs increased with dose. Light and electron microscopy of the lung tissue verified the presence of nanoparticles, free in the alveolar space and within phagosomes of macrophages not attached to alveolar epithelium. Chronification of local acute alveolitis was supported by dose-dependent increase of macrophage count in the alveolar region, oedema and thickening of interstitium, and increased expression of certain pro-inflammatory cytokines (interleukin-1a, LIX, L-selectin, vascular endothelial growth factor). Oxidative stress and lipid peroxidation increased substantially in the treated rats' lungs, and correlation was found between Ti content and lipid peroxidation. Insufficiency of the alveolar epithelial and capillary endothelial barrier was indicated by nanoparticle-laden phagocytes in hilar lymph nodes, suggesting nanoparticles reaching systemic circulation and distant organs, inducing systemic acute inflammation. Conclusion: TiO2 nanoparticles, reaching lower airways, may be etiological factors in the causation or aggravation of pulmonary diseases with acute and chronic airways inflammation and/or progressive fibrosis and obstruction (e.g., chronic obstructive pulmonary disease or asthma). Autophagy and damaged immune response (lymphocytic activity) may have here a role.

Original languageHungarian
Pages (from-to)57-66
Number of pages10
JournalOrvosi Hetilap
Volume160
Issue number2
DOIs
Publication statusPublished - jan. 1 2019

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Nanotubes
Nanoparticles
Lung
Lipid Peroxidation
Electron Microscopy
Oxidative Stress
Epithelium
Lymph Nodes
Macrophages
Body Weight
Metal Nanoparticles
Cytokines
Inflammation
L-Selectin
Light
Phagosomes
Nanotechnology
Organ Size
Interleukins
Autophagy

Keywords

  • Cytokines
  • Nanoparticles
  • Oxidative stress
  • Pathology
  • Rat
  • Titanium dioxide

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Titán-dioxid-nanopálcikák tüdore kifejtett hatásának állatkísérletes vizsgálata szubakut patkánymodellben. / Horváth, Tamara; Papp, A.; Kiricsi, Mónika; Igaz, Nóra; Trenka, Vivien; Kozma, Gábor; Tiszlavicz, L.; Rázga, Zsolt; Vezér, Tünde.

In: Orvosi Hetilap, Vol. 160, No. 2, 01.01.2019, p. 57-66.

Research output: Article

Horváth, Tamara ; Papp, A. ; Kiricsi, Mónika ; Igaz, Nóra ; Trenka, Vivien ; Kozma, Gábor ; Tiszlavicz, L. ; Rázga, Zsolt ; Vezér, Tünde. / Titán-dioxid-nanopálcikák tüdore kifejtett hatásának állatkísérletes vizsgálata szubakut patkánymodellben. In: Orvosi Hetilap. 2019 ; Vol. 160, No. 2. pp. 57-66.
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abstract = "Introduction: The development of nanotechnology increases the risk of occupational and population-level exposure to nanoparticles nowadays. However, scientifically based knowledge relating to the toxicity of heavy metal nanoparticles and potential health damage is insufficient. Aim: Investigation of lung tissue damage induced by titanium dioxide (TiO2) nanorods in subacute intratracheal instillation by morphological, chemical and biochemical methods in rat model. Method: General toxicity (changes of body and organ weights), local acute and chronic cellular toxicity (in alveolar spaces and epithelium, in hilar lymph nodes) and oxidative stress were examined using light and electron microscopy, and biochemical methods (reactive oxygen species, lipid peroxidation, expression of pro-inflammatory cytokines). Results: No dose- and time-dependent alteration was found in the body weight of the treated groups; but the mass and Ti content of lungs increased with dose. Light and electron microscopy of the lung tissue verified the presence of nanoparticles, free in the alveolar space and within phagosomes of macrophages not attached to alveolar epithelium. Chronification of local acute alveolitis was supported by dose-dependent increase of macrophage count in the alveolar region, oedema and thickening of interstitium, and increased expression of certain pro-inflammatory cytokines (interleukin-1a, LIX, L-selectin, vascular endothelial growth factor). Oxidative stress and lipid peroxidation increased substantially in the treated rats' lungs, and correlation was found between Ti content and lipid peroxidation. Insufficiency of the alveolar epithelial and capillary endothelial barrier was indicated by nanoparticle-laden phagocytes in hilar lymph nodes, suggesting nanoparticles reaching systemic circulation and distant organs, inducing systemic acute inflammation. Conclusion: TiO2 nanoparticles, reaching lower airways, may be etiological factors in the causation or aggravation of pulmonary diseases with acute and chronic airways inflammation and/or progressive fibrosis and obstruction (e.g., chronic obstructive pulmonary disease or asthma). Autophagy and damaged immune response (lymphocytic activity) may have here a role.",
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T1 - Titán-dioxid-nanopálcikák tüdore kifejtett hatásának állatkísérletes vizsgálata szubakut patkánymodellben

AU - Horváth, Tamara

AU - Papp, A.

AU - Kiricsi, Mónika

AU - Igaz, Nóra

AU - Trenka, Vivien

AU - Kozma, Gábor

AU - Tiszlavicz, L.

AU - Rázga, Zsolt

AU - Vezér, Tünde

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Introduction: The development of nanotechnology increases the risk of occupational and population-level exposure to nanoparticles nowadays. However, scientifically based knowledge relating to the toxicity of heavy metal nanoparticles and potential health damage is insufficient. Aim: Investigation of lung tissue damage induced by titanium dioxide (TiO2) nanorods in subacute intratracheal instillation by morphological, chemical and biochemical methods in rat model. Method: General toxicity (changes of body and organ weights), local acute and chronic cellular toxicity (in alveolar spaces and epithelium, in hilar lymph nodes) and oxidative stress were examined using light and electron microscopy, and biochemical methods (reactive oxygen species, lipid peroxidation, expression of pro-inflammatory cytokines). Results: No dose- and time-dependent alteration was found in the body weight of the treated groups; but the mass and Ti content of lungs increased with dose. Light and electron microscopy of the lung tissue verified the presence of nanoparticles, free in the alveolar space and within phagosomes of macrophages not attached to alveolar epithelium. Chronification of local acute alveolitis was supported by dose-dependent increase of macrophage count in the alveolar region, oedema and thickening of interstitium, and increased expression of certain pro-inflammatory cytokines (interleukin-1a, LIX, L-selectin, vascular endothelial growth factor). Oxidative stress and lipid peroxidation increased substantially in the treated rats' lungs, and correlation was found between Ti content and lipid peroxidation. Insufficiency of the alveolar epithelial and capillary endothelial barrier was indicated by nanoparticle-laden phagocytes in hilar lymph nodes, suggesting nanoparticles reaching systemic circulation and distant organs, inducing systemic acute inflammation. Conclusion: TiO2 nanoparticles, reaching lower airways, may be etiological factors in the causation or aggravation of pulmonary diseases with acute and chronic airways inflammation and/or progressive fibrosis and obstruction (e.g., chronic obstructive pulmonary disease or asthma). Autophagy and damaged immune response (lymphocytic activity) may have here a role.

AB - Introduction: The development of nanotechnology increases the risk of occupational and population-level exposure to nanoparticles nowadays. However, scientifically based knowledge relating to the toxicity of heavy metal nanoparticles and potential health damage is insufficient. Aim: Investigation of lung tissue damage induced by titanium dioxide (TiO2) nanorods in subacute intratracheal instillation by morphological, chemical and biochemical methods in rat model. Method: General toxicity (changes of body and organ weights), local acute and chronic cellular toxicity (in alveolar spaces and epithelium, in hilar lymph nodes) and oxidative stress were examined using light and electron microscopy, and biochemical methods (reactive oxygen species, lipid peroxidation, expression of pro-inflammatory cytokines). Results: No dose- and time-dependent alteration was found in the body weight of the treated groups; but the mass and Ti content of lungs increased with dose. Light and electron microscopy of the lung tissue verified the presence of nanoparticles, free in the alveolar space and within phagosomes of macrophages not attached to alveolar epithelium. Chronification of local acute alveolitis was supported by dose-dependent increase of macrophage count in the alveolar region, oedema and thickening of interstitium, and increased expression of certain pro-inflammatory cytokines (interleukin-1a, LIX, L-selectin, vascular endothelial growth factor). Oxidative stress and lipid peroxidation increased substantially in the treated rats' lungs, and correlation was found between Ti content and lipid peroxidation. Insufficiency of the alveolar epithelial and capillary endothelial barrier was indicated by nanoparticle-laden phagocytes in hilar lymph nodes, suggesting nanoparticles reaching systemic circulation and distant organs, inducing systemic acute inflammation. Conclusion: TiO2 nanoparticles, reaching lower airways, may be etiological factors in the causation or aggravation of pulmonary diseases with acute and chronic airways inflammation and/or progressive fibrosis and obstruction (e.g., chronic obstructive pulmonary disease or asthma). Autophagy and damaged immune response (lymphocytic activity) may have here a role.

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KW - Nanoparticles

KW - Oxidative stress

KW - Pathology

KW - Rat

KW - Titanium dioxide

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