HYDROGEN PEROXIDE, OXYGEN, SUPEROXIDE ANION, SINGLET OXYGEN AND PEROXIDASE

1979 ◽  
pp. 167-176 ◽  
Author(s):  
H.B. Dunford
Keyword(s):  
Hydrogen Peroxide ◽  
Singlet Oxygen ◽  
Superoxide Anion

Biochemical Oxygen Activation as the Basis for the Physiological Action of Tetrachlorodecaoxide (TCDO)

1985 ◽  
Vol 40 (5-6) ◽  
pp. 409-414 ◽  
Author(s):  
R. J. Youngman ◽  
G. R. Wagner ◽  
F. W. Kühne ◽  
E. F. Elstner
Keyword(s):  
Hydrogen Peroxide ◽  
Superoxide Dismutase ◽  
Singlet Oxygen ◽  
Protein Complex ◽  
Superoxide Anion ◽  
Carbonic Acid ◽  
Oxygen Species ◽  
Compound I ◽  
Activated Oxygen ◽  
Oxidation Of Methionine

Abstract Oxidation of methionine, 4-(methylthio)-2-oxobutyric acid (KMB), or 1-aminocyclopropane carbonic acid (ACC) are indicator reactions for activated oxygen species such as singlet oxygen (1O2), OH·-radical like oxidants, superoxide anion (O2·-), hydrogen peroxide (H2O2) or activated hemo-iron complexes like peroxidase-or catalase-“compound”. Methionine is oxidized by OH· as well as by 102 forming ethylene, but not by tetrachloro-decaoxygen complex (TCDO) in the absence or presence of catalytic hemoproteins such as peroxidase, hemoglobin or myoglobin. Both KMB and ACC are oxidized by TCDO under the catalysis of the above hemo-proteins where neither catalase nor superoxide dismutase are inhibitors. TCDO hemo-protein complex is an oxidant with similar properties as peroxidase-compound I and can clearly be differentiated from 02·-, H2O2, OH· and 1O2.

scholarly journals Suurstoftoksisiteit

1990 ◽  
Vol 9 (3) ◽  
pp. 118-123
Author(s):  
C. A. Van der Westhuizen ◽  
M. Viljoen ◽  
M. J. Pitout ◽  
P. H. Van Papendorp
Keyword(s):  
Hydrogen Peroxide ◽  
Endoplasmic Reticulum ◽  
Hydroxyl Radical ◽  
Singlet Oxygen ◽  
Superoxide Anion ◽  
Energy Production ◽  
Plasma Membranes ◽  
The Body ◽  
Toxic Metabolites ◽  
Oxygen Metabolites

Oxygen has been discovered about 200 years ago. Since then the vital physiological involvement of oxygen in various biologi­cal processes, mainly energy production, has been established. However, in the body molecular oxygen can be converted to toxic oxygen metabolites such as superoxide anion, hydrogen peroxide, the hydroxyl radical and singlet oxygen. These toxic metabolites are produced mainly in the mitochondria, plasma membranes and endoplasmic reticulum.

Oxidation of hydrogen peroxide at the dropping mercury electrode

1984 ◽  
Vol 49 (10) ◽  
pp. 2320-2331 ◽  
Author(s):  
Miroslav Březina ◽  
Martin Wedell
Keyword(s):  
Hydrogen Peroxide ◽  
Superoxide Anion ◽  
Ph Value ◽  
Mercury Electrode ◽  
Electrode Process ◽  
Electrochemical Processes ◽  
Dropping Mercury Electrode ◽  
Oxidation Of Hydrogen ◽  
Decreasing Ph ◽  
Rate Controlling Step

Reduction of oxygen and oxidation of hydrogen peroxide at the dropping mercury electrode are electrochemical processes strongly influenced both by the pH value and the anions in solution. With decreasing pH, both processes become irreversible, especially in the presence of anions with a negative φ2 potential of the diffusion part of the double layer. In the case of irreversible oxygen reduction, the concept that the rate-controlling step of the electrode process is the acceptance of the first electron with the formation of the superoxide anion, O2-, was substantiated. Oxidation of hydrogen peroxide becomes irreversible at a lower pH value than the reduction of oxygen. The slowest, i.e. rate-controlling step of the electrode process in borate buffers at pH 9-10 is the transfer of the second electron, i.e. oxidation of superoxide to oxygen.

Factors which affect DNA strand breakage in human leukocytes exposed to a tumor promoter, phorbol myristate acetate

1982 ◽  
Vol 60 (11) ◽  
pp. 1359-1366 ◽  
Author(s):  
H. C. Birnboim
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Phorbol Myristate Acetate ◽  
Respiratory Burst ◽  
Superoxide Anion ◽  
Tumor Promoter ◽  
Myristate Acetate ◽  
Strand Breakage ◽  
Dna Strand ◽  
Dna Strand Breakage

We have recently reported that phorbol myristate acetate (PMA) induces extensive DNA strand break damage in human peripheral blood leukocytes. The mechanism of action involves superoxide anion and hydrogen peroxide which are generated by phagocytes during the "respiratory burst." In this report, we describe the effect of various inhibitors and scavengers on PMA-induced DNA damage. Azide and cyanide greatly increased the level of damage; sulfhydryl compounds (glutathione, cysteine, and cysteamine) and ascorbate markedly decreased the level of damage. Hydroxyl radical scavengers such as dimethyl sulfoxide (DMSO) and glycerol also decreased the level of damage but apparently did so by inhibiting the respiratory burst. Diethyldithiocarbamate (DDC) increased the level of DNA damage at low concentrations (<1 mM), but decreased DNA damage at ≥1 mM. The results are consistent with a mechanism involving superoxide anion and hydrogen peroxide, but the precise reaction (free radical or enzymatic) responsible for DNA strand breakage has not been determined. The PMA-stimulated phagocyte is an interesting model system for looking at "active oxygen" mediated DNA damage and factors which influence it.

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