scholarly journals Involvement of an NAD(P)H oxidase-like enzyme in superoxide anion and hydrogen peroxide generation by rat type II cells

Thorax ◽  
1997 ◽  
Vol 52 (5) ◽  
pp. 465-471 ◽  
Author(s):  
R. J. van Klaveren ◽  
C. Roelant ◽  
M. Boogaerts ◽  
M. Demedts ◽  
B. Nemery
Keyword(s):  
Hydrogen Peroxide ◽  
Superoxide Anion ◽  
Type Ii Cells ◽  
Type Ii ◽  
Hydrogen Peroxide Generation

scholarly journals Presence of the distinct systems responsible for superoxide anion and hydrogen peroxide generation in red tide phytoplankton Chattonella marina and Chattonella ovata

2007 ◽  
Vol 29 (3) ◽  
pp. 241-247 ◽  
Author(s):  
Daekyung Kim ◽  
Takuji Nakashima ◽  
Yukihiko Matsuyama ◽  
Yoshimi Niwano ◽  
Kenichi Yamaguchi ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Superoxide Anion ◽  
Red Tide ◽  
Chattonella Marina ◽  
Hydrogen Peroxide Generation

Impairment of sodium-coupled uptakes by hydrogen peroxide in alveolar type II cells: protective effect of d-alpha-tocopherol

1992 ◽  
Vol 262 (5) ◽  
pp. L542-L548 ◽  
Author(s):  
C. Clerici ◽  
G. Friedlander ◽  
C. Amiel
Keyword(s):  
Hydrogen Peroxide ◽  
Atpase Activity ◽  
Protective Effect ◽  
Atp Depletion ◽  
Alpha Tocopherol ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Dependent Manner ◽  
Type Ii ◽  
Alveolar Type Ii Cells

Hydrogen peroxide (H2O2) is likely to play an important role in oxidant alveolar epithelium injury. We investigated the effect of H2O2 on uptake of phosphate, alanine in cultured rat alveolar type II cells. H2O2 induced inhibition of Na-dependent component of phosphate and alanine uptakes in time- and concentration-dependent manner. Twenty minutes exposure to 2.5 mM H2O2 decreased the maximum velocity (Vmax) of phosphate and alanine uptake by 50 and 62%, respectively, whereas Michaelis constant (Km) values were unchanged. H2O2 also decreased Na-K-ATPase activity, measured by ouabain-sensitive rubidium influx, and this effect was independent of H2O2-induced ATP depletion. A lipid-soluble antioxidant, d-alpha-tocopherol (20 microM, 24 h), prevented H2O2-induced decrease in Na-coupled uptake and Na-K-ATPase activity. These results indicate that H2O2 affects Na-dependent phosphate and alanine uptakes and suggest that this effect may be related at least, in part, to a decrease in Na transmembrane gradient, since H2O2 also affects Na-K-ATPase activity. The protective effect of d-alpha-tocopherol suggests that peroxidation of the membrane lipids is likely to be involved in the observed effects.

scholarly journals Discrete Generation of Superoxide and Hydrogen Peroxide by T Cell Receptor Stimulation

2002 ◽  
Vol 195 (1) ◽  
pp. 59-70 ◽  
Author(s):  
Satish Devadas ◽  
Luba Zaritskaya ◽  
Sue Goo Rhee ◽  
Larry Oberley ◽  
Mark S. Williams
Keyword(s):  
Hydrogen Peroxide ◽  
T Cell ◽  
T Cell Receptor ◽  
Superoxide Anion ◽  
Fas Ligand ◽  
Interleukin 2 ◽  
Cell Receptor ◽  
Activated T Cells ◽  
Tcr Signals ◽  
Hydrogen Peroxide Generation

Receptor-stimulated generation of reactive oxygen species (ROS) has been shown to regulate signal transduction, and previous studies have suggested that T cell receptor (TCR) signals may involve or be sensitive to ROS. In this study, we have shown for the first time that TCR cross-linking induced rapid (within 15 min) generation of both hydrogen peroxide and superoxide anion, as defined with oxidation-sensitive dyes, selective pharmacologic antioxidants, and overexpression of specific antioxidant enzymes. Furthermore, the data suggest the novel observation that superoxide anion and hydrogen peroxide are produced separately by distinct TCR-stimulated pathways. Unexpectedly, TCR-stimulated activation of the Fas ligand (FasL) promoter and subsequent cell death was dependent upon superoxide anion, but independent of hydrogen peroxide, while nuclear factor of activated T cells (NFAT) activation or interleukin 2 transcription was independent of all ROS. Anti-CD3 induced phosphorylation of extracellular signal–regulated kinase (ERK)1/2 required hydrogen peroxide generation but was unaffected by superoxide anion. Thus, antigen receptor signaling induces generation of discrete species of oxidants that selectively regulate two distinct redox sensitive pathways, a proapoptotic (FasL) and a proliferative pathway (ERK).

Inhibition of poly(ADP-ribose) polymerase preserves surfactant synthesis after hydrogen peroxide exposure

1995 ◽  
Vol 269 (1) ◽  
pp. L59-L64 ◽  
Author(s):  
B. B. Hudak ◽  
J. Tufariello ◽  
J. Sokolowski ◽  
C. Maloney ◽  
B. A. Holm
Keyword(s):  
Hydrogen Peroxide ◽  
Oxidant Stress ◽  
Type Ii Cells ◽  
Type Ii ◽  
Energy Depletion ◽  
Pharmacological Agents ◽  
Type Ii Pneumocytes ◽  
Type Ii Cell ◽  
Parp Activity

Exposure to hydrogen peroxide (H2O2) decreases phosphatidylcholine (PC) synthesis in rabbit type II pneumocytes. Activation of poly(ADP-ribose) polymerase (PARP) may play a role in this process. Exposure of type II pneumocytes to H2O2 resulted in a 53% decrease in the rate of incorporation of [3H]choline into PC (P < 0.001). Cell NAD and ATP levels were decreased by 52% (P < 0.001) and 39% (P < 0.01), respectively, without significant changes in cell viability. Exposure to H2O2 also resulted in a 52% (P < 0.05) increase in the activity of PARP. Preincubation of type II cells with inhibitors of PARP (nicotinamide; 3-aminobenzamide) before H2O2 exposure prevented the increase in PARP activity, and blocked the decreases in ATP, NAD, and rate of PC synthesis. These results suggest that the energy depletion associated with activation of PARP contributes to the effects of oxidant stress on type II cell metabolic function and may be ameliorated by pharmacological agents in vitro.

Metabolic changes in alveolar type II cells after exposure to hydrogen peroxide

1990 ◽  
Vol 259 (2) ◽  
pp. L57-L65 ◽  
Author(s):  
L. B. LaCagnin ◽  
L. Bowman ◽  
J. Y. Ma ◽  
P. R. Miles
Keyword(s):  
Hydrogen Peroxide ◽  
Energy State ◽  
Lactate Production ◽  
Atp Synthesis ◽  
Major Effect ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Isolated Lung

Since oxygen metabolites may play an important role in pulmonary oxidant injury, the effects of hydrogen peroxide (H2O2) on energy metabolism in alveolar type II cells isolated from rats were studied. The major effect of H2O2 is a rapid and dramatic reduction in the steady-state level of cellular ATP; e.g., ATP levels are reduced by 77 +/- 3% after only 5 min of exposure to H2O2 (0.5 mM). Cellular oxygen consumption is affected in a similar manner, suggesting that ATP synthesis is impaired. Experiments with isolated lung mitochondria demonstrate that exposure to 0.5 mM H2O2 for 5 min inhibits the rate of mitochondrial ATP synthesis by 51 +/- 3%. The site of mitochondrial ATP synthesis inhibition by H2O2 appears to be the adenosinetriphosphatase-synthase enzyme complex which phosphorylates ADP to ATP. Mitochondrial electron transport is unaffected. The association of 3-O-methylglucose with type II cells and glycolytic metabolism, measured as lactate production, are reduced by 25-35% by H2O2. The data also show that the cells are capable of recovery following exposure to H2O2, at least at lower exposure levels. These results indicate that exposure of type II cells to H2O2 alters the energy state of the cells by decreasing ATP synthesis. In turn, other important cellular functions may be impaired.

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