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Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium.

Publication ,  Journal Article
Beaver, LM; Stemmy, EJ; Constant, SL; Schwartz, A; Little, LG; Gigley, JP; Chun, G; Sugden, KD; Ceryak, SM; Patierno, SR
Published in: Toxicol Appl Pharmacol
February 15, 2009

Certain particulate hexavalent chromium [Cr(VI)] compounds are human respiratory carcinogens that release genotoxic soluble chromate, and are associated with fibrosis, fibrosarcomas, adenocarcinomas and squamous cell carcinomas of the lung. We postulate that inflammatory processes and mediators may contribute to the etiology of Cr(VI) carcinogenesis, however the immediate (0-24 h) pathologic injury and immune responses after exposure to particulate chromates have not been adequately investigated. Our aim was to determine the nature of the lung injury, inflammatory response, and survival signaling responses following intranasal exposure of BALB/c mice to particulate basic zinc chromate. Factors associated with lung injury, inflammation and survival signaling were measured in airway lavage fluid and in lung tissue. A single chromate exposure induced an acute immune response in the lung, characterized by a rapid and significant increase in IL-6 and GRO-alpha levels, an influx of neutrophils, and a decline in macrophages in lung airways. Histological examination of lung tissue in animals challenged with a single chromate exposure revealed an increase in bronchiolar cell apoptosis and mucosal injury. Furthermore, chromate exposure induced injury and inflammation that progressed to alveolar and interstitial pneumonitis. Finally, a single Cr(VI) challenge resulted in a rapid and persistent increase in the number of airways immunoreactive for phosphorylation of the survival signaling protein Akt, on serine 473. These data illustrate that chromate induces both survival signaling and an inflammatory response in the lung, which we postulate may contribute to early oncogenesis.

Duke Scholars

Published In

Toxicol Appl Pharmacol

DOI

EISSN

1096-0333

Publication Date

February 15, 2009

Volume

235

Issue

1

Start / End Page

47 / 56

Location

United States

Related Subject Headings

  • Toxicology
  • Time Factors
  • Proto-Oncogene Proteins c-akt
  • Particle Size
  • Mice, Inbred BALB C
  • Mice
  • Lung Diseases
  • Inhalation Exposure
  • Inflammation
  • Gene Expression Regulation
 

Citation

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Beaver, L. M., Stemmy, E. J., Constant, S. L., Schwartz, A., Little, L. G., Gigley, J. P., … Patierno, S. R. (2009). Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium. Toxicol Appl Pharmacol, 235(1), 47–56. https://doi.org/10.1016/j.taap.2008.11.018
Beaver, Laura M., Erik J. Stemmy, Stephanie L. Constant, Arnold Schwartz, Laura G. Little, Jason P. Gigley, Gina Chun, Kent D. Sugden, Susan M. Ceryak, and Steven R. Patierno. “Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium.Toxicol Appl Pharmacol 235, no. 1 (February 15, 2009): 47–56. https://doi.org/10.1016/j.taap.2008.11.018.
Beaver LM, Stemmy EJ, Constant SL, Schwartz A, Little LG, Gigley JP, et al. Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium. Toxicol Appl Pharmacol. 2009 Feb 15;235(1):47–56.
Beaver, Laura M., et al. “Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium.Toxicol Appl Pharmacol, vol. 235, no. 1, Feb. 2009, pp. 47–56. Pubmed, doi:10.1016/j.taap.2008.11.018.
Beaver LM, Stemmy EJ, Constant SL, Schwartz A, Little LG, Gigley JP, Chun G, Sugden KD, Ceryak SM, Patierno SR. Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium. Toxicol Appl Pharmacol. 2009 Feb 15;235(1):47–56.
Journal cover image

Published In

Toxicol Appl Pharmacol

DOI

EISSN

1096-0333

Publication Date

February 15, 2009

Volume

235

Issue

1

Start / End Page

47 / 56

Location

United States

Related Subject Headings

  • Toxicology
  • Time Factors
  • Proto-Oncogene Proteins c-akt
  • Particle Size
  • Mice, Inbred BALB C
  • Mice
  • Lung Diseases
  • Inhalation Exposure
  • Inflammation
  • Gene Expression Regulation