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Hyperoxia‐induced Cell Death in the Lung‐the Correlation of Apoptosis, Necrosis, and Inflammation
Author(s) -
MANTELL LIN L.,
HOROWITZ STUART,
DAVIS JONATHAN M.,
KAZZAZ JEFFREY A.
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb07931.x
Subject(s) - hyperoxia , apoptosis , lung , necrosis , inflammation , programmed cell death , medicine , pathology , immunology , biology , biochemistry
ABSTRACT 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.