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Am J Physiol Lung Cell Mol Physiol (March 29, 2002). doi:10.1152/ajplung.00012.2002
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Articles in PresS, published online ahead of print March 29, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00012.2002
Submitted on January 10, 2002
Accepted on March 23, 2002

Oxidative stress and inflammation contribute to lung toxicity following a common breast-cancer chemotherapy regimen

Amir M Abushamaa1, Thomas A Sporn2, and Rodney J Folz3*

1 Department of Medicine, Duke University Medical Center, Durham, NC, USA
2 Department of Pathology, Duke University Medical Center, Durham, NC, USA
3 Department of Medicine, Duke University Medical Center, Durham, NC, USA; Department of Cell Biology, Duke University Medical Center, Durham, NC, USA

* To whom correspondence should be addressed. E-mail: rodney.folz{at}duke.edu.

Delayed pulmonary toxicity syndrome (DPTS) following high-dose chemotherapy (HDC) and autologous hematopoetic support occurs in up to 64% of women with advanced stage breast cancer. Using a similar, but non myeloablative 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, BAL lipid peroxidation and BAL total cell counts. Most interestingly at 6 weeks BAL total cell counts had increased 4-fold with lymphocyte cell counts increasing more than 11-fold. A single supplemental dose of glutathione prevented early lung injury at 48 hours but showed no lung protective effects at 6 weeks, whereas single doses of other thiol sparing agents (ethyol and glutathione monethyl 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 following the use of these chemotherapeutic agents.




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