Oxygen poisoning of NAD biosynthesis: A proposed site of cellular oxygen toxicity

Experiments were performed on rats to determine whether the protection which anesthesia (sodium pentobarbital) affords against convulsions in oxygen at high pressure (OHP) of 70–75 psi extends to the pulmonary damage and, if so, whether such protection is due simply to the depression of general metabolism. These experiments showed that anesthesia protected against both the pulmonary damage and the convulsions and that this protection was equally well pronounced whether the metabolic depression was or was not counteracted and elevated by dinitrophenol, L-thyronine, or direct tetanic stimulation of muscle. The results support the conclusion that such protection is not due simply to the depression of general metabolism as has been claimed. They also imply that the potentiation of pulmonary damage in OHP by thyroid and CO2 is not a direct effect but rather is of central origin. The close association between the pulmonary damage and convulsions in OHP justifies the inference that these effects are not separate entities, as has been claimed, and point to the importance of central and neurogenic factors in the causation of this pulmonary damage. hyperbaric oxygenation; oxygen poisoning at high pressure; oxygen convulsion in relation to pulmonary damage; pulmonary edema and congestion in oxygen at high pressure; neurogenic factors and toxicity of oxygen at high pressure; direct and neurogenic effects of oxygen at high pressure on the lungs; pCO2and oxygen poisoning; thyroid and pulmonary damage in oxygen poisoning; protection against oxygen toxicity by pentobarbital, urethan, alpha chloralose, and propylene glycol Submitted on September 11, 1964

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Relative susceptibility of altitude-acclimatized mice to acute oxygen toxicity

Journal of Applied Physiology ◽

10.1152/jappl.1975.38.2.279 ◽

1975 ◽

Vol 38 (2) ◽

pp. 279-281

Author(s):

P. Hall ◽

C. L. Schatte ◽

J. W. Fitch

Keyword(s):

High Pressures ◽

Oxygen Toxicity ◽

High Energy ◽

Gamma Aminobutyric Acid ◽

Time To Death ◽

Relative Susceptibility ◽

Buffer Base ◽

The Times ◽

Log Linear ◽

Oxygen Poisoning

The influence of hypoxic acclimatization at altitudes of 0, 5,000, or 15,000 ft on the relative susceptibility to acute oxygen poisoning was determined in 288 adult female mice. After acclimatization periods of 1, 2, 4, or 8 wk, the mice were exposed to oxygen at high pressures (OHP) of 4, 6, or 9 ATA and the times to convulsion and death recorded. A factorial analysis of variance indicated that altitude and OHP level had inverse, log-linear effects on both parameters. The duration of acclimatization progressively decreased the time to death. The onset of convulsions and death was independent of body weight. There were significant interactions on the measured parameters between various combinations of altitude, OHP level, and duration of acclimatization. While alterations in the metabolism of gamma-aminobutyric acid and high-energy compounds are common to both hypoxia and hyperoxia, the most plausible explanation of the results relates to the decrease in buffer base induced by hypoxic acclimatization which might have caused CO2 potentiation of OHP symptoms.

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Electron paramagnetic resonance evidence that cellular oxygen toxicity is caused by the generation of superoxide and hydroxyl free radicals

FEBS Letters ◽

10.1016/0014-5793(89)80881-6 ◽

1989 ◽

Vol 252 (1-2) ◽

pp. 12-16 ◽

Cited By ~ 49

Author(s):

Jay L. Zweier ◽

Scherer S. Duke ◽

Periannan Kuppusamy ◽

J.T. Sylvester ◽

Edward W. Gabrielson

Keyword(s):

Electron Paramagnetic Resonance ◽

Free Radicals ◽

Oxygen Toxicity ◽

Paramagnetic Resonance ◽

Cellular Oxygen ◽

Electron Paramagnetic ◽

Hydroxyl Free Radicals

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Effect of Various Substances On Survival Times of Mice Exposed to Different High Oxygen Tensions

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1958.192.3.563 ◽

1958 ◽

Vol 192 (3) ◽

pp. 563-571 ◽

Cited By ~ 59

Author(s):

Rebeca Gerschman ◽

Daniel L. Gilbert ◽

Daniel Caccamise

Keyword(s):

Survival Time ◽

Detrimental Effect ◽

Calcium Salt ◽

Oxygen Toxicity ◽

Common Mechanism ◽

Survival Times ◽

Acid Sodium Salt ◽

X Irradiation ◽

Diethyldithiocarbamic Acid ◽

Oxygen Poisoning

Mice were exposed to various pressures of oxygen up to 10 atm. Survival times decreased abruptly between 0.7 and 1 atm. of oxygen, and reached a minimum value of 19 minutes at 10 atm. Cysteamine, reduced glutathione and thiourea had a detrimental effect at 1 or 1.5 atm. but protected mice at 6 atm. of oxygen. Cystamine and oxidized glutathione did not protect at 1 atm. but gave protection at 6 atm. of oxygen. AET (ß-aminoethylisothiuronium) gave no protection at 1 or 10 atm. but increased the survival time of mice exposed to 2 and 2.5 atm. Cobalt increased the survival time of mice exposed to 1 atm. and either exerted no influence or had a slight detrimental effect at higher oxygen pressures. Ca EDTA (calcium salt of ethylenediamintetraacetic acid) did not change the survival time of mice exposed to 6 atm. of oxygen. DEDTC (diethyldithiocarbamic acid sodium salt) increased the survival time of mice in 6 atm. of oxygen. Trihydroxyphenone antioxidants showed some protective effect against oxygen toxicity in mice exposed to 6 atm. of oxygen. The results are not inconsistent with the notion of a possible common mechanism between oxygen poisoning and x-irradiation. The action of any given agent was found to depend upon the oxygen pressure used.

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