 | MECHANISMS OF CELL DEATH: THE SECOND ANNUAL CONFERENCE OF THE CELL DEATH SOCIETY
Copyright © 1999 by the New York Academy of Sciences
description
Annals of the New York Academy of Sciences 887:171-180 (1999)
© 1999 New York Academy of Sciences
Hyperoxia-induced Cell Death in the Lung-the Correlation of Apoptosis, Necrosis, and Inflammation
LIN L. MANTELLa,b,e,
STUART HOROWITZd,
JONATHAN M. DAVISc AND
JEFFREY A. KAZZAZa
aCardioPulmonary Research Institute, Winthrop-University Hospital, SUNY/Stony Brook School of Medicine, Mineola, New York 11501, USA
bDepartment of Thoracic Cardiovascular Surgery, Winthrop-University Hospital, SUNY/Stony Brook School of Medicine, Mineola, New York 11501, USA
cDepartment of Pediatrics, Winthrop-University Hospital, SUNY/Stony Brook School of Medicine, Mineola, New York 11501, USA
dThe Heart and Lung Institute, Jewish Hospital, Louisville, Kentucky 40202, USA
eAddress for correspondence: CardioPulmonary Research Institute, Winthrop-University Hospital, 222 Station Plaza North, Suite 505, Mineola, NY 11501; 516-663-8978 (voice); 516-663-8872 (fax). e-mail: lmantell{at}winthrop.org
Prolonged exposure to hyperoxia causes tissue damage in many organs and tissues. Since the entire surface area of lung epithelium is directly exposed to O 2 and other inhaled agents, hyperoxia leads to the development of both acute and chronic lung injuries.These pathologic changes in the lung can also be seen in acute lung injury (ALI) in response to other agents. Simple strategies to mitigate hyperoxia-induced ALI might not be effective by virtue of merely reducing or augmenting the extent of apoptosis of pulmonary cells. Identification of the specific cell types undergoing apoptosis and further understanding of the precise timing of the onset of apoptosis may be necessary in order to gain a greater understanding of the connection between apoptosis and tolerance to hyperoxia and ALI. Attention should also be focused on other forms of non-apoptotic programmed cell death.
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