Effects of tocopherols, methylene blue and glutathione on the manifestations of oxygen poisoning in vitamin E‐deficient rats

Taylor, D. W.

doi:10.1113/jphysiol.1958.sp005914

Cited by 33 publications

(9 citation statements)

References 6 publications

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“…Our experi~lleilts with erythrocytes ill an atmosphere of pure oxygen confirmed the observatio~ls of others (14,15,16) that heillolysis can take place slowly under these conditions. Again, the degree of he~llolysis paralleled the level of lipid peroxides formed.…”

Section: Discussionsupporting

confidence: 91%

“…Raiha (15) noted hemolysis of human erythrocytes incubated with oxygen, and found that administration of tocopherol, 1 day before the blood was drawn, inhibited this henlolysis. Taylor (16) studied the effect of high oxygen pressure (5 atnlospheres) on hemolysis of rat erythrocytes in vivo, and found that large doses of tocopherol were required for protection against hemolysis. Injection of glutathione also afforded some protection.…”

Section: Lipid Peroxidation and Iiernolysis Under A N Oxygen Atmospherementioning

confidence: 99%

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The Protective Action of Tocopherol Against Hemolysis of Rat Erythrocytes by Dialuric Acid

Tsen

Collier

1960

Can. J. Biochem. Physiol.

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Erythrocytes from rats on tocopherol-deficient and tocopherol-supplemented diets gave similar low values for lipid peroxides by the thiobarbituric acid test. Treatment of the cells from tocopherol-deficient rats with dialuric acid caused a marked increase in lipid peroxitles and this closely paralleled the degree of hernolysis. Shaking of the red cells from tocopherol-deficient arlimals in a n atmosphere of oxygen also resulted in a slow lipid peroxidatio~l which again paralleled the degree of hernolysis. Addition of a-tocopherol to a suspension of erythrocytes from tocopherol-deficient rats decreased or completely prevented (depending upon concentration) hemolysis by dialuric acid and also decreased lipid peroxitle formation.It is concluded that dialuric acid probably acts by catalyzing the formation of lipid peroxides in the unsaturated lipids of the membrane of erythrocytes from tocopherol-deficient animals. Tocopherol presumably inhibits peroxide formation, and therefore hemolysis, by virtue of its antioxidant action.

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Section: Discussionsupporting

confidence: 91%

Section: Lipid Peroxidation and Iiernolysis Under A N Oxygen Atmospherementioning

confidence: 99%

The Protective Action of Tocopherol Against Hemolysis of Rat Erythrocytes by Dialuric Acid

Tsen

Collier

1960

Can. J. Biochem. Physiol.

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“…Since no tocopherol assays were performed on erythrocytes, plasma, or other tissues of these mice, the question of their tocopherol status merits comment. Excellent evidence of their tocopherol deficiency was provided by the accentuated lysis and lipid peroxidation of their erythrocytes by hydrogen peroxide, as compared to normal mouse erythrocytes (11,13,14,19). Whereas susceptibility to lipid peroxidation can be increased by diet-induced alterations in composition of erythrocyte lipid, specifically by an increase in erythrocyte unsaturated fatty acid content, this was unlikely in these experiments since the diet contained 10%o lard rather than unsaturated fatty acids.…”

Section: Methodsmentioning

confidence: 86%

“…Studies in this laboratory and in others have linked in vitro peroxidation of erythrocyte lipid and hemolysis (11)(12)(13)(14)(15)(16)(17)(18). Some observations had suggested that oxidation of unsaturated fatty acids might occur in vivo (11,19,20). However, to date the occurrence of lipid peroxidation in vivo has not been unequivocally demonstrated, and therefore its biologic significance has not been established.…”

mentioning

confidence: 99%

Effects of in vivo hyperoxia on erythrocytes. 3. In vivo peroxidation of erythrocyte lipid.

Mengel¹,

Kann²

1966

J. Clin. Invest.

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“…Although the relationship of SOD to bronchopulmonary dysplasia is not clearly understood, measurement of red cell S O D activity in red cells may reflect a response to intrapulmonary exposure to 0,-radicals and provide a mechanism f o r their removal while the red cell is in close proximity to the alveolar wall. Oxygen induced lung damage has bccn associated with oxygen-induced hemolysis (44). In the present study, we have ( I ) compared cord blood levels of red cell S O D over a range of gestational ages and (2) compared the S O D response of premature infants with RDS exposed to oxygcn over 72 hr of therapy with gestational age-matched premature infants without RDS over a sinlilar 72-hr period; and (3) evaluated the relationship of red cell SOD enzyme activity over a 72-hr period to the develop ment of pulmonary oxygen toxicity in infants treated for RDS.…”

Section: Speculationmentioning

confidence: 99%

Neonatal Red Cell Superoxide Dismutase Enzyme Levels: Possible Role as a Cellular Defense Mechanism against Pulmonary Oxygen Toxicity

1977

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Summaryof an unidentified factor in plasma for induction to be dcmonRed cell superoxide dismutase (SOD) enzyme activity was determined in 5 8 cord blood specinlens obtained from infants over a range of gestational ages. An inverse relationship between red cell S O D activity and gestational age was demonstrated. Red cell S O D activity showed a progressive fall from 263.1 k 30.5 units/mg non-hemoglobin protein (NIIP) in infants of less than 29 weeks of gestation to 168.9 +. 21.3 unitslmg N H P in infants of more than 36 weeks of gestation (P < 0.05).Infants treated for RDS showecl an increase in red cell S O D activity which reached significance at 72 hr when colnpared to cord blood levels from the same population ( P < 0.05). No similar significant difference could be demonstrated in gestational age-matched control subjects over the same time period. IIowever, initial cord blood S O D enzylne levels were lower in premature infants with RDS (229.5 k 30.6 unitslmg NI1P) than in premature infants without RDS (264.0 k 38.0 unitslmg ~1 1~) .When infants with RDS were exan~ined for oxygen toxicity and survival, red cell S O D levels were noted to decrease over 24 hr in four of five infants who died, three of whom developed bronchopul~nonary dysplasia. In the surviving infants, red cell S O D levels showed a significant increase by 4 8 hr ( P < 0.05).None developed bronchopulmonary dyplasia and all survived. SpeculationIncreases in red cell superoxide dis~liutase activity in response to hyperoxic stress may prevent toxic effects of 0,-radicals and oxygen toxicity to the lung.Oxygen is fundamental to survival of aerobic systems. However, in excess, molecular oxygcn has bccn associated with toxic tissue effects as noted in bronchopulmonary dysplasia (4,8,33,38) and retrolental fibroplasia (22). The complete reduction of 1 molecule of oxygen yields intern~ediates which include 0,-(superoxide radical), OH.(hydroxyl radical), and H,O, (24). Fridovich (12,13,17,18,25,40) and others (32) have recently proposed that a major part of oxygen toxicity at the cellular level may be mediated by the superoxide radical. All oxygen-metabolizing cells so far examined have been found to contain enzymes that catalyze the reaction: 0 , -+ 0 , -+ 2H+ + H,O, + 0,.These enzymes, which have been characterized as metalloproteins, are designated superoxide dismutases (1 2).Mammalian studies have only recently been attempted in an effort to delineate the relationship of SOD enzyme levels and the occurence of pulmonary oxygen toxicity (3,8,14). Decreased levels of lung SOD have been demonstrated in those infants dying from RDS (4, 38). Induction of enzyme activity has been observed in rat lungs after exposure to increased oxygen concentrations ( 3 , 8 , 14) and seems to be dependent upon the presence strated (3).The red cell provides an accessible source of human SOD. Although the relationship of SOD to bronchopulmonary dysplasia is not clearly understood, measurement of red cell S O D activity in red cells may reflect a response to intrapulmonary...

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Effects of tocopherols, methylene blue and glutathione on the manifestations of oxygen poisoning in vitamin E‐deficient rats

Cited by 33 publications

References 6 publications

The Protective Action of Tocopherol Against Hemolysis of Rat Erythrocytes by Dialuric Acid

The Protective Action of Tocopherol Against Hemolysis of Rat Erythrocytes by Dialuric Acid

Effects of in vivo hyperoxia on erythrocytes. 3. In vivo peroxidation of erythrocyte lipid.

Neonatal Red Cell Superoxide Dismutase Enzyme Levels: Possible Role as a Cellular Defense Mechanism against Pulmonary Oxygen Toxicity

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