Vitamin E Deficiency Enhances Pulmonary Inflammatory Response and Oxidative Stress Induced by Single-Walled Carbon Nanotubes in C57BL/6 Mice

Details

• Personal Author:
  Arepalli S ; Castranova, Vincent ; Gao F ; Gorelik O ; Kagan VE ; Kisin ER ; Murray AR ; Oury T ; Shvedova AA ; Tyurina YY ; Young SH
• Description:
  Exposure of mice to single walled carbon nanotubes (SWCNT) induces an unusually robust pulmonary inflammatory response with a very early onset of fibrosis, which is accompanied by a significant oxidative stress and antioxidant depletion. The role of specific components of the antioxidant protective system, specifically vitamin E, the major lipid-soluble antioxidant of membranes and lipoproteins, in the SWCNT induced reactions required further investigation. We used C57BL/6 mice, maintained on a vitamin E-sufficient diet as well as on a vitamin E-deficient diet, to explore and compare the pulmonary inflammatory reactions to aspired SWCNTs. The induced vitamin E-deficiency (a 90-fold depletion of á-tocopherol in the lung) resulted in a significant decline of other antioxidants as well as in accumulation of lipid peroxidation products. A more severe decrease of pulmonary antioxidants was detected in SWCNT treated vitamin E-deficient mice as compared to controls. Exposure of vitamin E-sufficient mice to SWCNTs markedly shifted the ratio of low to high molecular weight forms of extra-cellular SOD (EC-SOD) such that approximately 3-4 times greater amounts of this neutrophil-associated enzyme were present. This effect was enhanced in vitamin E-deficient animals. Lowered levels of antioxidants in vitamin E-deficient mice were associated with a higher sensitivity to SWCNT-induced acute inflammation (PMNs number, released LDH, protein content, pro-inflammatory cytokines level) as well as pro-fibrotic pathways (TGF-â elevation and collagen deposition). Given that pulmonary levels of vitamin E can be manipulated through diet, its effects on SWCNT responses may be of practical importance in optimizing protective anti-inflammatory strategies. [Description provided by NIOSH]
• Subjects:
  Animals Antioxidants Asthma Asthma, Occupational Dust Lung Metals Occupational Health Particulate Matter Respiratory System Respiratory Tract Diseases Safety

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• Keywords:
  Alveolar-cells Animal-studies Bronchial-asthma Fibrogenesis Metal-compounds Nanotechnology Particulate-dust Pulmonary-system-disorders Respirable-dust Respiratory-system-disorders Vitamins

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• ISSN:
  0041-008X
• Document Type:
  Text
• Funding:
  Grant
• Genre:
  Journal Article
• Place as Subject:
  OSHA Region 3 ; Pennsylvania ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Pages in Document:
  339-348
• Volume:
  221
• Issue:
  3
• NIOSHTIC Number:
  nn:20032071
• Citation:
  Toxicol Appl Pharmacol 2007 Jun; 221(3):339-348
• CAS Registry Number:
  Carbon (CAS RN 7440-44-0)
• Federal Fiscal Year:
  2007
• NORA Priority Area:
  Manufacturing
• Performing Organization:
  University of Pittsburgh at Pittsburgh
• Peer Reviewed:
  True
• Start Date:
  20050701
• Source Full Name:
  Toxicology and Applied Pharmacology
• End Date:
  20160630
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:0a347aadfe9aad102e5290138a0ac4cbc43af6200a59f515cc165a41a0b585cb809c82c25253b437ce9f04f1f5a8472824457c479100bd2b02447c3b0bd7e4be
• Download URL:
  https://stacks.cdc.gov/view/cdc/186138/cdc_186138_DS1.pdf
• File Type:
  [PDF - 960.63 KB ]