Hyperoxia-induced cell death in the lung - the correlation of apoptosis, necrosis, and inflammation

被引:97
作者
Mantell, LL
Horowitz, S
Davis, JM
Kazzaz, JA
机构
[1] SUNY Stony Brook, Winthrop Univ Hosp, Sch Med, CardioPulm Res Inst, Mineola, NY 11501 USA
[2] SUNY Stony Brook, Winthrop Univ Hosp, Sch Med, Dept Cardiovasc Thorac Surg, Mineola, NY 11501 USA
[3] SUNY Stony Brook, Winthrop Univ Hosp, Sch Med, Dept Pediat, Mineola, NY 11501 USA
[4] Jewish Hosp St Louis, Heart & Lung Inst, Louisville, KY 40202 USA
来源
MECHANISMS OF CELL DEATH: THE SECOND ANNUAL CONFERENCE OF THE CELL DEATH SOCIETY | 1999年 / 887卷
关键词
D O I
10.1111/j.1749-6632.1999.tb07931.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:171 / 180
页数:10
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