Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods

Abderrahim Nemmar, Khaled Melghit, Suhail Al-Salam, Shaheen Zia, Subramanian Dhanasekaran, Samir Attoub, Issa Al-Amri, Badreldin H. Ali

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Nanomaterials are extensively used in medicines, industry and daily life, but little is known about their possible health effects. Titanium dioxide (TiO2) nonmaterial-based photocatalysis is useful in the complete mineralization of organic pollutants in waste water and air. While the Fe-doping of TiO2 enhances their photocatalytic activity, their potential pathophysiologic effects are unknown. Here, rutile Fe-doped (9%) pure titanium dioxide (TiO2) nanorods were prepared and characterized. Subsequently, we assessed the acute (24h) pulmonary and extrapulmonary effects of intratracheal (i.t.) instillation of these nanorods (1 and 5mg/kg) in Wistar rats. In the bronchoalveolar lavage, the treatment induced a significant and dose-dependent increase of neutrophils, an increase of interleukin-6 (IL-6, at 5mg/kg), and caused a dose-dependent-decrease of superoxide dismutase (SOD) activity. The lung sections of rats exposed to rutile Fe-TiO2 nanorods showed infiltration of inflammatory cells in dose-dependent manner. Similarly, the heart rate, systolic blood pressure, plasma IL-6, and leukocyte and platelet numbers were increased at 5mg/kg. The plasma SOD and reduced glutathaione activities were dose-dependently decreased after exposure to the nanorods. Histopathologically, the liver showed mild inflammatory cells infiltration of few portal tracts, but the kidneys and heart were unaffected. In plasma, the levels of lactate dehydrogenase and hepatic enzymes, i.e., alanine aminotranferease and aspartate aminotransferase were increased significantly. The in vitro exposure of human lung cancer cells NCI-H460-Luc2 and human hepatoma cells HepG2 to FeTiO2 (6.25-100μg/ml) dose-dependently reduced cellular viability. Also, the In vitro direct addition of these nanorods (0.1-1μg/ml) to untreated rat blood, significantly and dose-dependently induced platelet aggregation. In conclusion, exposure to rutile Fe-TiO2 promotes pulmonary and systemic inflammation and oxidative stress. It affects the liver, enhances thrombotic potential, heart rate and systolic blood pressure. Moreover, the rutile Fe-TiO2 elicited direct toxicity on NCI-H460-Luc2 and HepG2 cells.

Original languageEnglish
Pages (from-to)167-175
Number of pages9
JournalToxicology
Volume279
Issue number1-3
DOIs
Publication statusPublished - Jan 11 2011

Fingerprint

Nanotubes
Nanorods
Toxicity
Lung
Blood Pressure
Rats
Interleukin-6
Blood pressure
Hep G2 Cells
Platelets
Plasmas
Infiltration
Liver
Superoxide Dismutase
Heart Rate
Oxidative stress
Nanostructures
Photocatalysis
Organic pollutants
Bronchoalveolar Lavage

Keywords

  • Cell lines
  • Liver
  • Lung
  • Nanoparticulate
  • Nanotechnology
  • Toxicity

ASJC Scopus subject areas

  • Toxicology

Cite this

Nemmar, A., Melghit, K., Al-Salam, S., Zia, S., Dhanasekaran, S., Attoub, S., ... Ali, B. H. (2011). Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods. Toxicology, 279(1-3), 167-175. https://doi.org/10.1016/j.tox.2010.10.007

Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods. / Nemmar, Abderrahim; Melghit, Khaled; Al-Salam, Suhail; Zia, Shaheen; Dhanasekaran, Subramanian; Attoub, Samir; Al-Amri, Issa; Ali, Badreldin H.

In: Toxicology, Vol. 279, No. 1-3, 11.01.2011, p. 167-175.

Research output: Contribution to journalArticle

Nemmar, A, Melghit, K, Al-Salam, S, Zia, S, Dhanasekaran, S, Attoub, S, Al-Amri, I & Ali, BH 2011, 'Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods', Toxicology, vol. 279, no. 1-3, pp. 167-175. https://doi.org/10.1016/j.tox.2010.10.007
Nemmar A, Melghit K, Al-Salam S, Zia S, Dhanasekaran S, Attoub S et al. Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods. Toxicology. 2011 Jan 11;279(1-3):167-175. https://doi.org/10.1016/j.tox.2010.10.007
Nemmar, Abderrahim ; Melghit, Khaled ; Al-Salam, Suhail ; Zia, Shaheen ; Dhanasekaran, Subramanian ; Attoub, Samir ; Al-Amri, Issa ; Ali, Badreldin H. / Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods. In: Toxicology. 2011 ; Vol. 279, No. 1-3. pp. 167-175.
@article{3382c624bb35430da14bb1dc3ebac50c,
title = "Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods",
abstract = "Nanomaterials are extensively used in medicines, industry and daily life, but little is known about their possible health effects. Titanium dioxide (TiO2) nonmaterial-based photocatalysis is useful in the complete mineralization of organic pollutants in waste water and air. While the Fe-doping of TiO2 enhances their photocatalytic activity, their potential pathophysiologic effects are unknown. Here, rutile Fe-doped (9{\%}) pure titanium dioxide (TiO2) nanorods were prepared and characterized. Subsequently, we assessed the acute (24h) pulmonary and extrapulmonary effects of intratracheal (i.t.) instillation of these nanorods (1 and 5mg/kg) in Wistar rats. In the bronchoalveolar lavage, the treatment induced a significant and dose-dependent increase of neutrophils, an increase of interleukin-6 (IL-6, at 5mg/kg), and caused a dose-dependent-decrease of superoxide dismutase (SOD) activity. The lung sections of rats exposed to rutile Fe-TiO2 nanorods showed infiltration of inflammatory cells in dose-dependent manner. Similarly, the heart rate, systolic blood pressure, plasma IL-6, and leukocyte and platelet numbers were increased at 5mg/kg. The plasma SOD and reduced glutathaione activities were dose-dependently decreased after exposure to the nanorods. Histopathologically, the liver showed mild inflammatory cells infiltration of few portal tracts, but the kidneys and heart were unaffected. In plasma, the levels of lactate dehydrogenase and hepatic enzymes, i.e., alanine aminotranferease and aspartate aminotransferase were increased significantly. The in vitro exposure of human lung cancer cells NCI-H460-Luc2 and human hepatoma cells HepG2 to FeTiO2 (6.25-100μg/ml) dose-dependently reduced cellular viability. Also, the In vitro direct addition of these nanorods (0.1-1μg/ml) to untreated rat blood, significantly and dose-dependently induced platelet aggregation. In conclusion, exposure to rutile Fe-TiO2 promotes pulmonary and systemic inflammation and oxidative stress. It affects the liver, enhances thrombotic potential, heart rate and systolic blood pressure. Moreover, the rutile Fe-TiO2 elicited direct toxicity on NCI-H460-Luc2 and HepG2 cells.",
keywords = "Cell lines, Liver, Lung, Nanoparticulate, Nanotechnology, Toxicity",
author = "Abderrahim Nemmar and Khaled Melghit and Suhail Al-Salam and Shaheen Zia and Subramanian Dhanasekaran and Samir Attoub and Issa Al-Amri and Ali, {Badreldin H.}",
year = "2011",
month = "1",
day = "11",
doi = "10.1016/j.tox.2010.10.007",
language = "English",
volume = "279",
pages = "167--175",
journal = "Toxicology",
issn = "0300-483X",
publisher = "Elsevier Ireland Ltd",
number = "1-3",

}

TY - JOUR

T1 - Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods

AU - Nemmar, Abderrahim

AU - Melghit, Khaled

AU - Al-Salam, Suhail

AU - Zia, Shaheen

AU - Dhanasekaran, Subramanian

AU - Attoub, Samir

AU - Al-Amri, Issa

AU - Ali, Badreldin H.

PY - 2011/1/11

Y1 - 2011/1/11

N2 - Nanomaterials are extensively used in medicines, industry and daily life, but little is known about their possible health effects. Titanium dioxide (TiO2) nonmaterial-based photocatalysis is useful in the complete mineralization of organic pollutants in waste water and air. While the Fe-doping of TiO2 enhances their photocatalytic activity, their potential pathophysiologic effects are unknown. Here, rutile Fe-doped (9%) pure titanium dioxide (TiO2) nanorods were prepared and characterized. Subsequently, we assessed the acute (24h) pulmonary and extrapulmonary effects of intratracheal (i.t.) instillation of these nanorods (1 and 5mg/kg) in Wistar rats. In the bronchoalveolar lavage, the treatment induced a significant and dose-dependent increase of neutrophils, an increase of interleukin-6 (IL-6, at 5mg/kg), and caused a dose-dependent-decrease of superoxide dismutase (SOD) activity. The lung sections of rats exposed to rutile Fe-TiO2 nanorods showed infiltration of inflammatory cells in dose-dependent manner. Similarly, the heart rate, systolic blood pressure, plasma IL-6, and leukocyte and platelet numbers were increased at 5mg/kg. The plasma SOD and reduced glutathaione activities were dose-dependently decreased after exposure to the nanorods. Histopathologically, the liver showed mild inflammatory cells infiltration of few portal tracts, but the kidneys and heart were unaffected. In plasma, the levels of lactate dehydrogenase and hepatic enzymes, i.e., alanine aminotranferease and aspartate aminotransferase were increased significantly. The in vitro exposure of human lung cancer cells NCI-H460-Luc2 and human hepatoma cells HepG2 to FeTiO2 (6.25-100μg/ml) dose-dependently reduced cellular viability. Also, the In vitro direct addition of these nanorods (0.1-1μg/ml) to untreated rat blood, significantly and dose-dependently induced platelet aggregation. In conclusion, exposure to rutile Fe-TiO2 promotes pulmonary and systemic inflammation and oxidative stress. It affects the liver, enhances thrombotic potential, heart rate and systolic blood pressure. Moreover, the rutile Fe-TiO2 elicited direct toxicity on NCI-H460-Luc2 and HepG2 cells.

AB - Nanomaterials are extensively used in medicines, industry and daily life, but little is known about their possible health effects. Titanium dioxide (TiO2) nonmaterial-based photocatalysis is useful in the complete mineralization of organic pollutants in waste water and air. While the Fe-doping of TiO2 enhances their photocatalytic activity, their potential pathophysiologic effects are unknown. Here, rutile Fe-doped (9%) pure titanium dioxide (TiO2) nanorods were prepared and characterized. Subsequently, we assessed the acute (24h) pulmonary and extrapulmonary effects of intratracheal (i.t.) instillation of these nanorods (1 and 5mg/kg) in Wistar rats. In the bronchoalveolar lavage, the treatment induced a significant and dose-dependent increase of neutrophils, an increase of interleukin-6 (IL-6, at 5mg/kg), and caused a dose-dependent-decrease of superoxide dismutase (SOD) activity. The lung sections of rats exposed to rutile Fe-TiO2 nanorods showed infiltration of inflammatory cells in dose-dependent manner. Similarly, the heart rate, systolic blood pressure, plasma IL-6, and leukocyte and platelet numbers were increased at 5mg/kg. The plasma SOD and reduced glutathaione activities were dose-dependently decreased after exposure to the nanorods. Histopathologically, the liver showed mild inflammatory cells infiltration of few portal tracts, but the kidneys and heart were unaffected. In plasma, the levels of lactate dehydrogenase and hepatic enzymes, i.e., alanine aminotranferease and aspartate aminotransferase were increased significantly. The in vitro exposure of human lung cancer cells NCI-H460-Luc2 and human hepatoma cells HepG2 to FeTiO2 (6.25-100μg/ml) dose-dependently reduced cellular viability. Also, the In vitro direct addition of these nanorods (0.1-1μg/ml) to untreated rat blood, significantly and dose-dependently induced platelet aggregation. In conclusion, exposure to rutile Fe-TiO2 promotes pulmonary and systemic inflammation and oxidative stress. It affects the liver, enhances thrombotic potential, heart rate and systolic blood pressure. Moreover, the rutile Fe-TiO2 elicited direct toxicity on NCI-H460-Luc2 and HepG2 cells.

KW - Cell lines

KW - Liver

KW - Lung

KW - Nanoparticulate

KW - Nanotechnology

KW - Toxicity

UR - http://www.scopus.com/inward/record.url?scp=78649993929&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78649993929&partnerID=8YFLogxK

U2 - 10.1016/j.tox.2010.10.007

DO - 10.1016/j.tox.2010.10.007

M3 - Article

C2 - 21073913

AN - SCOPUS:78649993929

VL - 279

SP - 167

EP - 175

JO - Toxicology

JF - Toxicology

SN - 0300-483X

IS - 1-3

ER -