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(Received for publication, March 22, 1996)
From the CardioPulmonary Research Institute and the
ABSTRACT All forms of aerobic life are faced with the
threat of oxidation from molecular oxygen (O2) and have
evolved antioxidant defenses to cope with this potential problem.
However, cellular antioxidants can become overwhelmed by oxidative
insults, including supraphysiologic concentrations of O2
(hyperoxia). Oxidative cell injury involves the modification of
cellular macromolecules by reactive oxygen intermediates (ROI), often
leading to cell death. O2 therapy, which is a widely used
component of life-saving intensive care, can cause lung injury. It is
generally thought that hyperoxia injures cells by virtue of the
accumulation of toxic levels of ROI, including
H2O2 and the superoxide anion
(O INTRODUCTION All aerobic life forms face the threat of oxidation from molecular
oxygen (O2) (1, 2). Perhaps to cope with this threat,
families of enzymatic and nonenzymatic antioxidants have evolved (3).
Antioxidants prevent the accumulation of toxic levels of oxygen-derived
free radicals, also called reactive oxygen intermediates
(ROI),1 which can wreak havoc upon cells by
modifying proteins (4), lipids (5), and DNA (6). Yet because
O2 is vital to human life, O2 therapy is used
in the treatment of critically ill patients who cannot breath
efficiently. These patients often require supraphysiologic
concentrations of O2 (>21%) to maintain organ viability
(7). However, hyperoxia is toxic to normal cells and organisms (5), and
the lungs of such patients can be damaged, probably because lungs
receive the highest O2 exposure (7, 8).
Cell culture experiments indicate that cells are usually killed
when exposed to >40% O2 (9). Exposure to hyperoxia is
associated with increased levels of ROI (2), which is reflected by the
accumulation of oxidatively damaged cellular macromolecules (1, 10, 11)
and chromosomal breakage (12). In cultured, transformed alveolar
epithelial cells, lethal exposure to hyperoxia (95% O2) is
also associated with cell cycle arrest at G2 (13) and
inactivation of aconitase (14). Presumably, hyperoxia causes cell
injury because cellular antioxidant defenses become overwhelmed (8),
leading to the accumulation of toxic levels of ROI. Cells can also be
injured directly by ROI. For example, exposure of cells to
H2O2 or superoxide radicals can result in cell
death (1, 5, 15). In the cases in which it has been examined, cell
death caused by these oxidants appears to occur via apoptosis, also
known as programmed cell death (16, 17, 18, 19, 20). This mode of cell death is
characterized by cell shrinkage, and in nucleated cells, by chromosome
condensation together with internucleosomal cleavage of DNA (21).
O2 toxicity is often considered to be similar to other
oxidant stresses. If hyperoxic cell death results from the accumulation
of ROI, then cells that die of hyperoxia might be predicted to die via
apoptosis. Indeed, the time frame in which hyperoxia kills cells is on
the order of days, certainly adequate time for the expression of
apoptosis-related genes. We report that, surprisingly, apoptosis is not
a characteristic event leading up to the death of epithelial cells by
hyperoxia. Rather, direct O2 toxicity appears to result in
necrosis. Paradoxically, apoptosis is a notable feature of hyperoxic
lung injury in vivo.
MATERIALS AND METHODS Human lung adenocarcinoma A549 cells (ATCC CCL
185) were grown in F12K medium (Life Technologies, Inc.) supplemented
with 10% heat-inactivated fetal bovine serum, 2 mM
glutamine, 100 units/ml penicillin, and 100 µg/ml streptomycin. Cells
were maintained at 37 °C in 95% room air, 5% CO2 in a
humidified chamber. Subconfluent cultures were used in all experiments,
and cells adhered overnight prior to experimental treatment. Cells were
cultured in sealed chambers flushed with 95% O2, 5%
CO2. Control cells were cultured in 95% room air, 5%
CO2. Some cell cultures were treated with
H2O2 or paraquat (Sigma). At
each time point, cell viability was determined by the exclusion of
Trypan blue dye and counted using a hemacytometer. Media and oxidants
were refreshed each day when cells were cultured for several days.
Cells were seeded on coverslips and
treated in an identical manner as in the cytotoxicity assay. The
protocol utilized for the TUNEL ( Tissue sections (4-5 µm) were mounted onto slides pretreated with
3-aminopropylethoxysilane (Digene Diagnostics, Inc., Beltsville, MD).
Slides were baked for 30 min at 60 °C and then washed twice in fresh
xylenes for 5 min each to remove paraffin. The slides were rehydrated
through a series of graded alcohols and then washed in distilled water
for 3 min in each. For TUNEL staining of the tissue sections, the
proteinase K treatment (30 µg/ml for 15 min) was included and the
sections were double-labeled with 2 µg/ml
4 For electron microscopy assays, cell cultures were fixed in 2.5%
glutaraldehyde in 0.1 M sodium cacodylate buffer (pH 7.2)
for 1 h at 4 °C. The cells were then postfixed in 1% osmium
tetroxide, dehydrated in a graded series of ethanol, and embedded in
LX112 (Ladd Corp., Burlington, VT). Thin sections (60 nm) were cut,
stained with uranyl acetate and lead citrate, and examined on a Zeiss
EM 10 transmission electron microscope.
Male C57 Bl/6J mice (8 to 10 weeks of age) were exposed to 100% O2 in plexiglass
chambers as described previously (22). Controls were kept in room air.
Animals were killed by cervical dislocation, and lungs were fixed by
perfusion of 10% buffered formalin at 20 cm H2O pressure
and embedded in paraffin as described previously (22).
Conditions were established enabling
apoptotic nuclei to be unambiguously and objectively scored by
computer-assisted image analysis using the Image 1 system (Universal
Imaging, West Chester, PA). At least 1000 nuclei were counted from a
minimum of two independent experiments for each time point. Between 10 and 50 random viewing fields were counted on each coverslip. To
quantify the extent of apoptosis, cells were dual-labeled with
rhodamine-conjugated anti-digoxigenin for TUNEL and Hoechst 33258. The total number of nuclei was determined by Hoechst dye fluorescence
using the UV-2A filter (Nikon Inc., Melville, NY), and TUNEL-positive
nuclei were evident with rhodamine fluorescence using the G-2A filter
(Nikon Inc.).
RESULTS Because the lung is a sensitive target of O2 toxicity,
we focused on a lung epithelial cell model. A549 cells, derived from
alveolar type II cells, have been extensively studied with respect to
their responses to hyperoxia and other oxidant injuries (14, 19). Cells
were cultured either in 95% room air or 95% O2. Table
I indicates that cells cultured in hyperoxia showed
overt signs of death (Trypan blue exclusion) by day 4 and were 69%
dead by day 7. The remainder of the cells died over the next 3 days
(data not shown). The kinetics of A549 cell death in hyperoxia are
similar to those reported for other cell types (23, 24, 25). Because cell
death from other oxidants occurs via apoptosis (16, 17, 18), we tested
whether hyperoxia also induces apoptosis.
Measurement of cell death and apoptosis
Volume 271, Number 25,
Issue of June 21, 1996
pp. 15182-15186
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
OXIDANT INJURY WITHOUT APOPTOSIS*
,
Department of Medicine (Nephrology), Winthrop-University
Hospital, State University of New York at Stony Brook School of
Medicine, Mineola, New York 11501
2), which are not adequately scavenged by
endogenous antioxidant defenses. These oxidants are cytotoxic and have
been shown to kill cells via apoptosis, or programmed cell death. If
hyperoxia-induced cell death is a result of increased ROI, then
O2 toxicity should kill cells via apoptosis. We studied
cultured epithelial cells in 95% O2 and assayed apoptosis
using a DNA-binding fluorescent dye, in situ end-labeling
of DNA, and electron microscopy. Using all approaches we found that
hyperoxia kills cells via necrosis, not apoptosis. In contrast, lethal
concentrations of either H2O2 or
O2 cause apoptosis. Paradoxically, apoptosis is a
prominent event in the lungs of animals injured by breathing 100%
O2. These data indicate that O2 toxicity is
somewhat distinct from other forms of oxidative injury and suggest that
apoptosis in vivo is not a direct effect of
O2.
erminal transferase
dTP ick nd-abeling)
staining of tissue sections was as described previously (22) except
that proteinase K treatment was omitted. TUNEL reagents including
rhodamine-conjugated anti-digoxigenin Fab fragment were obtained from
Boehringer Mannheim. Cells were double-labeled with 2 µg/ml Hoechst
33258 (Polysciences, Warrington, PA) for 2 min at room temperature.
,6-diamidine-2-phenylindole-dihydrochloride (Boehringer
Mannheim).
Treatment
% Cell death
AI (Hoechst)
AI (TUNEL)
95% O2
2 days
1.25
± 1.25
0.81 ± 0.32
1.60 ± 0.56
4 days
11.00 ± 7.00
0.69 ± 0.27
3.00
± 0.65
7 days
68.75 ± 4.77
0.36
± 0.21
2.80 ± 0.65
H2O2 (5 mM)
76.00 ± 1.16
62.90 ± 2.04
78.30
± 2.27
PQ (20 mM)
70.30 ± 1.67
71.70
± 2.50
67.40 ± 2.20
H2O2 (1 mM)
2 days
28.00 ± 5.00
0.56
± 0.27
ND
3 days
40.00
± 2.00
0.33 ± 0.24
ND
4
days
46.00 ± 5.00
0.10 ± 0.10
ND
PQ (20 µM)
3 days
4.00
± 4.00
0
ND
4
days
18.00
± 2.50
0
ND
5
days
32.50
± 3.50
0
ND
ABSTRACTOne means of determining the number of cells undergoing apoptosis in
cell culture utilizes the DNA-binding dye Hoechst 33258, which
fluoresces brightly under UV excitation when bound. Nuclei that are
condensed during apoptosis are much smaller and brighter than those in
nonapoptotic cells. Fig. 1 shows that the nuclei of
cells exposed to hyperoxia were larger than controls with no apparent
increase in fluorescent staining. In contrast, cells exposed to the
oxidants H2O2 or paraquat (which generates
intracellular O2) underwent apoptosis,
as shown by their characteristically shrunken and intensely-fluorescent
nuclei (Fig. 1).
Fig. 1. Apoptosis in hyperoxia, O2 and H2O2. A549 cells were double labeled with Hoechst 33258 (panels A-D) and TUNEL-labeled with rhodamine conjugated anti-digoxigenin antibody (panels E-H). Panels A and E represent a typical field of cells cultured under normal conditions. Panels B and F represent a typical field of cells exposed to 95% O2 for 7 days. The brightly stained cell in panel F is one of the rarely seen apoptotic cells when cells are exposed to hyperoxia. Panels C and G represent a typical field of cells exposed to 10 mM H2O2 for 4 h. Panels D and H represent a typical field of cells exposed to 20 mM paraquat for 18 h. Magnification bar represents 150 µm.
We also utilized the in situ TUNEL assay to study apoptosis
in these cultures. This assay labels 3-OH ends of DNA in chromatin,
which result from endonucleolytic cleavage occurring during apoptosis
(26, 27). Fig. 1 shows that cells cultured in hyperoxia were TUNEL
negative. In contrast, a large population of cells exposed to the other
oxidants was clearly TUNEL positive.
Another means of assessing whether cells are apoptotic is to study
their morphology by electron microscopy. Fig. 2 shows
that when cells were exposed to 95% O2 for 6 days they
became swollen, with enlarged nuclei and mitochondria. By contrast,
cells that were exposed to paraquat or H2O2 had
condensed chromatin, which is a hallmark of apoptosis. These data
confirm the results obtained using light microscopy and further
indicate that hyperoxia did not result in apoptosis.
Fig. 2. Electron micrographs of cells in hyperoxia, O2 and H2O2. Panel A, untreated cells; panel B, cells exposed to 95% O2 for 6 days; panel C, cells exposed to 5 mM H2O2 for 4 h; panel D, cells cultured in 5 mM paraquat for 18 h. The arrows show lamellar bodies characteristic of type II cells. Scale bar represents 1 µm.
If the kinetics of cell death is correlated with the extent of apoptosis at each time point, it may be concluded that the cells have died via apoptosis. Conversely, if there is no correlation, cells would have died via necrosis, not apoptosis. To quantify the extent of apoptosis, we used computer-aided image analysis. Fig. 1 shows that when apoptosis was induced by exposure to H2O2 or paraquat (panels C and D), a large population of cells with shrunken and brightly fluorescent nuclei were clearly distinguished from untreated cells (panel A). Using this approach, we established an objective threshold for the area of apoptotic nuclei. Cells were scored as apoptotic only when their nuclear area was beneath that threshold. Similar quantitative analyses have been achieved by fluorescence-activated cell sorting of nonadherent cells (28), although we have found that computer-aided image analysis is well suited to adherent cells. Table I shows that there was no correlation between cell death and the extent of apoptosis at any time during hyperoxic exposure, as determined either by image analysis after Hoechst staining or by counting TUNEL-positive nuclei. In contrast, cell death and apoptosis were tightly correlated in cultures exposed either to 5 mM H2O2 or 20 mM paraquat.
Hyperoxic cell death is also different than death from other oxidants in terms of the kinetics of cell killing. At the oxidant doses typically studied (6, 17, 18, 29, 30) and used here, cells are killed in a matter of hours, while it took days for hyperoxia. To determine if oxidant-induced apoptosis occurs when the rate of cell death is substantially reduced, experiments were performed at much lower concentrations of H2O2 and paraquat. Similar to cell death by hyperoxia, we observed virtually no apoptosis at much lower oxidant concentrations (see Table I). It should be noted that unlike hyperoxia, these low oxidant doses were not 100% lethal, and a subpopulation of cells began to adapt and divide (data not shown).
After determining that apoptosis did not occur in cells exposed to
hyperoxia in vitro, we became interested in hyperoxic lung
injury in vivo. Mice were exposed to 100% O2
for 48 h, a time at which they begin showing overt signs of lung
injury (22). TUNEL assays of tissue sections were used to assess
apoptosis in the lungs. Fig. 3 shows a typical result
with an obvious increase in the number of TUNEL-positive nuclei in the
hyperoxic lung. Therefore, in contrast to direct exposure of cells in
culture to hyperoxia, apoptosis was clearly induced in the lungs of
hyperoxic mice in vivo.
Fig. 3. Apoptosis in hyperoxia-injured lungs. Sections of lungs from control (panels A and C) and hyperoxic (panels B and D) mice. Panel A, section of a control lung stained with 4
,6-diamidine-2-phenylindole-dihydrochloride to visualize all the
nuclei; panel C, TUNEL staining of the same section showing
very few apoptotic, TUNEL-positive nuclei; panel B, section
of a hyperoxic lung (48 h in 100% O2) stained with
4,6-diamidine-2-phenylindole-dihydrochloride; panel D,
TUNEL staining of the same area showing widespread apoptosis.
Magnification bar represents 150 µm.
DISCUSSION
Apoptosis appears to be the major mode of cell death when cells
experience lethal oxidative insult from exposure to oxidants, including
H2O2 and superoxide (16, 17, 18, 19, 20). Interestingly,
even cells that undergo apoptosis following nonoxidative insults, such
as steroid treatment or viral infection, have been shown to accumulate
lipid peroxides, which is evidence of oxidative damage (31, 32, 33).
Moreover, apoptosis can be prevented in such cells by the
overexpression of cellular antioxidant enzymes or the oncogene
Bcl-2, which is thought to be an antioxidant
(34). Taken together, there is a tight correlation between oxidative
damage to cells and apoptosis, and lipid peroxidation may be a key step
leading to apoptosis in some cases and resulting from it in others. For
these reasons, we anticipated that another form of oxidant injury,
O2 toxicity, would also result in apoptosis. Hyperoxia is
lethal to cells and has been shown to cause the accumulation of
apoptosis-inducing reactive oxygen intermediates, such as
O2 and H2O2.
To test if hyperoxia causes apoptosis, we exposed alveolar epithelial
cells to 95% O2 and found that these cells did not die via
apoptosis. Using three assays, we found no evidence for apoptosis
caused by hyperoxia. We have made virtually identical observations in
HeLa cells (data not shown), suggesting that these results are
consistent in other epithelial cells and possibly in other cell types
as well. In sharp contrast, cells exposed to lethal concentrations of
two other oxidants, H2O2 or paraquat (which
generates intracellular O2), were
found to undergo typical apoptosis, consistent with previous
observations by others. Under the light microscope, hyperoxic cells and
their nuclei both appeared swollen. In EM, the mitochondria also
appeared swollen, and the chromatin was not condensed, although it was
highly condensed when the cells became apoptotic by other oxidants.
Overall, hyperoxic cells had a morphology typical of necrosis. The
simplest conclusion is that the mode of epithelial cell death by
hyperoxia is necrosis.
That apoptosis does not occur by molecular O2 but can occur by peroxide and superoxide radicals suggests that hyperoxia is distinct from other forms of lethal oxidative insult, causing a different mode of cell death. It is also likely that at least some of the organellar and macromolecular sites of O2 damage are different from sites affected by other oxidants, since molecular O2 is not as reactive as oxygen-derived free radicals, diffuses throughout the cell, and can target virtually all organelles and cytosolic molecules. One possible explanation for the lack of apoptosis in hyperoxia is that one or more steps in the oxidative damage-induced pathway to apoptosis might be sensitive to direct oxidation by high levels of molecular O2. This would predict that hyperoxia can inhibit apoptosis in some cases, which could be tested in mutant, hyperoxia-resistant cell lines. Consistent with this possibility is the observation that poly(A)DP-ribosylation is defective in hyperoxia-injured cells (35). Poly(A)DP-ribose polymerase must be activated by cleavage for apoptosis to occur in some systems (36). However, hyperoxia clearly does not inhibit apoptosis in all cases, since apoptosis occurs in lungs of animals injured by in vivo O2 toxicity.
The occurrence of apoptosis in hyperoxic lung is somewhat paradoxical, in light of the absence of apoptosis in cultured hyperoxic cells. Several possible explanations may account for this difference. First, the cell types that undergo apoptosis in lung have not yet been identified, and it is possible that nonepithelial cells become apoptotic. We believe that this is unlikely, however, since we have observed widespread apoptosis in many cell types of severely injured hyperoxic lungs, including airway and alveolar epithelium. Likewise, capillary endothelial cells, which appear to be the cell type most sensitive to hyperoxia in vivo, are described as becoming swollen during hyperoxic injury (37), consistent with cell death via necrosis. A second possibility is that apoptosis in hyperoxic lungs might require paracrine interactions or cell junctions among several cell types in the intact organ. A third and likely possibility is that apoptosis in hyperoxia-injured lung may be a downstream phenomenon, occurring as a result of the release of mediators that are known to induce apoptosis in some systems, or oxidants released by inflammatory cells. Supporting this notion is the observation that apoptosis occurs in a model of acute lung injury and inflammation (38).
When the dose of either H2O2 or paraquat was reduced to the point that the rate of cultured cell death was slowed considerably (from hours to days), the mode of cell death was changed, and many fewer cells underwent apoptosis. Moreover, the morphology of many of these cells was consistent with death via necrosis (data not shown). It is noteworthy that cell culture in low level oxidants is also associated with adaptation of clones or populations of cells, which maintain a selective advantage and continue to divide (39, 40). In contrast, this has not been shown to occur when unadapted cells are placed in 95% O2, which is uniformly lethal.
In summary, lethal exposure of cultured lung epithelial cells to hyperoxia causes cell necrosis. In contrast, exposure to high levels of the other oxidants, (H2O2 and superoxide), cause death via apoptosis, suggesting that lethal doses of O2 causes cell death via mechanisms that are distinct from death caused by lethal doses of other oxidants.
FOOTNOTES
§ To whom correspondence should be addressed: CardioPulmonary Research Inst., Ste. 604, Winthrop-University Hospital, 222 Station Pl. North, Mineola, NY 11501. Tel.: 516-663-3917; Fax: 516-663-8874; E-mail: sho1{at}aol.com.
1 The abbreviation used is: ROI, reactive oxygen intermediates.
Acknowledgments
We thank Drs. Marwan El-Sabban and John Maesaka for suggestions.
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O. Lesur, M. Brisebois, A. Thibodeau, F. Chagnon, D. Lane, and T. Fullop Role of IFN-{gamma} and IL-2 in rat lung epithelial cell migration and apoptosis after oxidant injury Am J Physiol Lung Cell Mol Physiol, January 1, 2004; 286(1): L4 - L14. [Abstract] [Full Text] [PDF]
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P. J. O'Reilly, J. M. Hickman-Davis, I. C. Davis, and S. Matalon Hyperoxia Impairs Antibacterial Function of Macrophages Through Effects on Actin Am. J. Respir. Cell Mol. Biol., April 1, 2003; 28(4): 443 - 450. [Abstract] [Full Text] [PDF]
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X. Zhang, P. Shan, M. Sasidhar, G. L. Chupp, R. A. Flavell, A. M. K. Choi, and P. J. Lee Reactive Oxygen Species and Extracellular Signal-Regulated Kinase 1/2 Mitogen-Activated Protein Kinase Mediate Hyperoxia-Induced Cell Death in Lung Epithelium Am. J. Respir. Cell Mol. Biol., March 1, 2003; 28(3): 305 - 315. [Abstract] [Full Text] [PDF]
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N. L. Parinandi, M. A. Kleinberg, P. V. Usatyuk, R. J. Cummings, A. Pennathur, A. J. Cardounel, J. L. Zweier, J. G. N. Garcia, and V. Natarajan Hyperoxia-induced NAD(P)H oxidase activation and regulation by MAP kinases in human lung endothelial cells Am J Physiol Lung Cell Mol Physiol, January 1, 2003; 284(1): L26 - L38. [Abstract] [Full Text] [PDF]
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S. A. McGrath-Morrow and J. Stahl Inhibition of Glutamine Synthetase in A549 Cells During Hyperoxia Am. J. Respir. Cell Mol. Biol., July 1, 2002; 27(1): 99 - 106. [Abstract] [Full Text] [PDF]
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C.-L. Wu, P. Domenico, D. J. Hassett, T. J. Beveridge, A. R. Hauser, and J. A. Kazzaz Subinhibitory Bismuth-Thiols Reduce Virulence of Pseudomonas aeruginosa Am. J. Respir. Cell Mol. Biol., June 1, 2002; 26(6): 731 - 738. [Abstract] [Full Text] [PDF]
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G. R. S. Budinger, M. Tso, D. S. McClintock, D. A. Dean, J. I. Sznajder, and N. S. Chandel Hyperoxia-induced Apoptosis Does Not Require Mitochondrial Reactive Oxygen Species and Is Regulated by Bcl-2 Proteins J. Biol. Chem., May 3, 2002; 277(18): 15654 - 15660. [Abstract] [Full Text] [PDF]
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K. H. Albertine and C. G. Plopper DNA Oxidation or Apoptosis . Will the Real Culprit of DNA Damage in Hyperoxic Lung Injury Please Stand Up? Am. J. Respir. Cell Mol. Biol., April 1, 2002; 26(4): 381 - 383. [Full Text] [PDF]
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R. L. Auten, M. H. Whorton, and S. Nicholas Mason Blocking Neutrophil Influx Reduces DNA Damage in Hyperoxia-Exposed Newborn Rat Lung Am. J. Respir. Cell Mol. Biol., April 1, 2002; 26(4): 391 - 397. [Abstract] [Full Text] [PDF]
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S. A. McGrath-Morrow and J. Stahl Apoptosis in Neonatal Murine Lung Exposed to Hyperoxia Am. J. Respir. Cell Mol. Biol., August 1, 2001; 25(2): 150 - 155. [Abstract] [Full Text] [PDF]
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A. M. Ilizarov, H.-C. Koo, J. A. Kazzaz, L. L. Mantell, Y. Li, R. Bhapat, S. Pollack, S. Horowitz, and J. M. Davis Overexpression of Manganese Superoxide Dismutase Protects Lung Epithelial Cells against Oxidant Injury Am. J. Respir. Cell Mol. Biol., April 1, 2001; 24(4): 436 - 441. [Abstract] [Full Text]
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C. Barazzone and C. W. White Mechanisms of Cell Injury and Death in Hyperoxia . Role of Cytokines and Bcl-2 Family Proteins Am. J. Respir. Cell Mol. Biol., May 1, 2000; 22(5): 517 - 519. [Full Text]
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N. S. Ward, A. B. Waxman, R. J. Homer, L. L. Mantell, O. Einarsson, Y. Du, and J. A. Elias Interleukin-6-Induced Protection in Hyperoxic Acute Lung Injury Am. J. Respir. Cell Mol. Biol., May 1, 2000; 22(5): 535 - 542. [Abstract] [Full Text]
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J. S. Shenberger and P. S. Dixon Oxygen Induces S-Phase Growth Arrest and Increases p53 and p21WAF1/CIP1 Expression in Human Bronchial Smooth-Muscle Cells Am. J. Respir. Cell Mol. Biol., September 1, 1999; 21(3): 395 - 402. [Abstract] [Full Text]
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Y.-j. Lee and E. Shacter Oxidative Stress Inhibits Apoptosis in Human Lymphoma Cells J. Biol. Chem., July 9, 1999; 274(28): 19792 - 19798. [Abstract] [Full Text] [PDF]
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W. R. Franek, S. Horowitz, L. Stansberry, J. A. Kazzaz, H.-C. Koo, Y. Li, Y. Arita, J. M. Davis, A. S. Mantell, W. Scott, et al. Hyperoxia Inhibits Oxidant-induced Apoptosis in Lung Epithelial Cells J. Biol. Chem., January 5, 2001; 276(1): 569 - 575. [Abstract] [Full Text] [PDF]
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