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Oxidative stress and inflammation contribute to lung toxicity after a common breast cancer chemotherapy regimen.

Publication ,  Journal Article
Abushamaa, AM; Sporn, TA; Folz, RJ
Published in: Am J Physiol Lung Cell Mol Physiol
August 2002

Delayed pulmonary toxicity syndrome after high-dose chemotherapy (HDC) and autologous hematopoietic support occurs in up to 64% of women with advanced-stage breast cancer. Using a similar, but nonmyeloablative, HDC treatment regimen in mice, we found both immediate and persistent lung injury, coincident with marked decreases in lung tissue glutathione reductase activity and accompanied by increases in lung oxidized glutathione, bronchoalveolar lavage (BAL) lipid peroxidation, and BAL total cell counts. Most interestingly, at 6 wk, BAL total cell counts had increased fourfold, with lymphocyte cell counts increasing >11-fold. A single supplemental dose of glutathione prevented early lung injury at 48 h but showed no lung-protective effects at 6 wk, whereas single doses of other thiol-sparing agents (Ethyol and glutathione monoethyl ester) showed no benefit. These data suggest that this HDC regimen results in acute and persistent lung toxicity, induced in part by oxidative stress, that culminates with an acute lung cellular inflammatory response. Continuous glutathione supplementation and/or attenuation of the delayed pulmonary inflammatory response may prove beneficial in preventing lung toxicity after the use of these chemotherapeutic agents.

Duke Scholars

Published In

Am J Physiol Lung Cell Mol Physiol

DOI

ISSN

1040-0605

Publication Date

August 2002

Volume

283

Issue

2

Start / End Page

L336 / L345

Location

United States

Related Subject Headings

  • Respiratory System
  • Pneumonia
  • Oxidative Stress
  • Mice, Inbred Strains
  • Mice
  • Lung
  • Lipid Peroxides
  • In Vitro Techniques
  • Glutathione Reductase
  • Glutathione Disulfide
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Abushamaa, A. M., Sporn, T. A., & Folz, R. J. (2002). Oxidative stress and inflammation contribute to lung toxicity after a common breast cancer chemotherapy regimen. Am J Physiol Lung Cell Mol Physiol, 283(2), L336–L345. https://doi.org/10.1152/ajplung.00012.2002
Abushamaa, Amir M., Thomas A. Sporn, and Rodney J. Folz. “Oxidative stress and inflammation contribute to lung toxicity after a common breast cancer chemotherapy regimen.Am J Physiol Lung Cell Mol Physiol 283, no. 2 (August 2002): L336–45. https://doi.org/10.1152/ajplung.00012.2002.
Abushamaa AM, Sporn TA, Folz RJ. Oxidative stress and inflammation contribute to lung toxicity after a common breast cancer chemotherapy regimen. Am J Physiol Lung Cell Mol Physiol. 2002 Aug;283(2):L336–45.
Abushamaa, Amir M., et al. “Oxidative stress and inflammation contribute to lung toxicity after a common breast cancer chemotherapy regimen.Am J Physiol Lung Cell Mol Physiol, vol. 283, no. 2, Aug. 2002, pp. L336–45. Pubmed, doi:10.1152/ajplung.00012.2002.
Abushamaa AM, Sporn TA, Folz RJ. Oxidative stress and inflammation contribute to lung toxicity after a common breast cancer chemotherapy regimen. Am J Physiol Lung Cell Mol Physiol. 2002 Aug;283(2):L336–L345.

Published In

Am J Physiol Lung Cell Mol Physiol

DOI

ISSN

1040-0605

Publication Date

August 2002

Volume

283

Issue

2

Start / End Page

L336 / L345

Location

United States

Related Subject Headings

  • Respiratory System
  • Pneumonia
  • Oxidative Stress
  • Mice, Inbred Strains
  • Mice
  • Lung
  • Lipid Peroxides
  • In Vitro Techniques
  • Glutathione Reductase
  • Glutathione Disulfide