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Journal of Clinical Investigation | 1967

Studies of Paroxysmal Nocturnal Hemoglobinuria Erythrocytes: Increased Lysis and Lipid Peroxide Formation by Hydrogen Peroxide*

Charles E. Mengel; Herbert E. Kann; Wilhelm D. Meriwether

When paroxysmal nocturnal hemoglobinuria (PNH) erythrocytes were exposed to H(2)O(2) they lysed excessively and formed greater than normal quantities of lipid peroxides when compared to red cells of normal subjects and patients with most types of hematologic disease. It was also shown that lytic sensitivity to acidified serum was related to the enhanced lytic sensitivity to H(2)O(2). If the lipid of PNH cells was first extracted then exposed to ultraviolet radiation more lipid peroxides were formed than in extracts of normal red blood cells. The possible explanations for these findings and their relationship to the PNH hemolytic mechanism are discussed.


Experimental Biology and Medicine | 1964

Effects of in vivo Hyperoxia on Erythrocytes 1. Hemolysis in Mice Exposed to Hyperbaric Oxygenation.

Charles E. Mengel; Herbert E. Kann; Wirt W. Smith; Betty D. Hokton

Summary In vivo lytic sensitivity of mouse erythrocytes to hyperbaric oxygenation paralleled their in vitro sensitivity to H2O2. In vitro lysis was associated with lipid peroxide formation. The in vivo and in vitro lysis and in vitro lipid peroxide formation were enhanced by vit. E deficiency and reduced by treatment of animals with a tocopherol acetate. It was suggested that hyperoxic hemolysis in vivo was a direct or indirect result of abnormal lipid peroxidation.


Annals of Internal Medicine | 1976

Ascorbic Acid Effects on Erythrocytes

Charles E. Mengel; Harry L. Greene

Excerpt To the editor: A recent communication in this journal (1) concerning a patient with G-6-PD deficiency who apparently suffered an episode of hemolysis after the administration of intravenous...


Experimental Biology and Medicine | 1965

EFFECTS OF IN VIVO HYPEROXIA ON ERYTHROCYTES. IV. STUDIES IN DOGS EXPOSED TO HYPERBARIC OXYGENATION.

Lewis G. Zirkle; Charles E. Mengel; Stephen A. Butler; Robert L. Fuson

Summary Erythrocytes of 20 dogs were studied before and after in vivo exposure to oxygen under high pressure (OHP). No evidence of in vivo hemolysis was noted but erythrocytes from dogs exposed to OHP demonstrated increased osmotic fragility and decreased acetylcholinesterase activity. Additional evidence indicated the in vivo formation of lipid peroxides in erythrocytes. No change in glucose-6-phosphate dehydrogenase activity, reduced glutathione content, or met-hemoglobin content occurred, and no Heinz bodies were formed during OHP. Thus, inadequacy of the pentose-phosphate shunt was probably not responsible for cell damage. It is suggested that altered permeability of erythrocytes resulted directly from peroxidation of lipids or indirectly from inhibition of erythrocyte acetylcholinesterase or a combination of both effects.


Journal of Clinical Investigation | 1972

In vivo formation of H2O2 in red cells during exposure to hyperoxia.

William P. Johnson; Devenia Jefferson; Charles E. Mengel

Chow-fed and tocopherol-deficient mice were given aminotriazole (AT), exposed to 100% O(2) at 60 pounds per square inch absolute for 1 hr (OHP), and red blood cells were assayed for catalase activity and lipid peroxide levels. A decrease of catalase activity (CA) in the presence of AT can be taken as evidence of excess formation or accumulation of H(2)O(2). No differences of CA were observed among chow-fed mice, with or without AT and/or OHP. Tocopherol-deficient mice with AT had lower CA (0.174+/-0.040) than chow-fed mice with AT (0.225+/-0.028) P < 0.01. Tocopherol-deficient mice with AT exposed to OHP had even lower CA, 0.137+/-0.024, P < 0.01.The data are consistent with the hypothesis that H(2)O(2) is formed or accumulated in excess in red cells of tocopherol-deficient mice, an effect that is enhanced in the presence of hyperoxia. They imply that tocopherol plays a role in the detoxification of H(2)O(2).


Annals of Internal Medicine | 1967

Paroxysmal Nocturnal Hemoglobinuria Obscured by the Presence of Iron Deficiency

Herbert E. Kann; Charles E. Mengel; Robert L. Wall

Excerpt In paroxysmal nocturnal hemoglobinuria (PNH) the loss of iron in the urine in the form of hemoglobin or hemosiderin is primarily responsible for the unusually high incidence of iron deficie...


Annals of Internal Medicine | 1988

Hydrochlorothiazide and Myalgias

Nagesh G. Kavi; Charles E. Mengel

Excerpt To the Editor:Hydrochlorothiazide is a commonly used diuretic and antihypertensive agent. Mild muscular symptoms with weakness, easy fatigability, and occasional cramps are common adverse r...


Biochemistry | 1966

Inhibition of erythrocyte acetylcholinesterase by peroxides.

Bert W. O'Malley; Charles E. Mengel; W. Delano Meriwether; Lewis G. Zirkle


JAMA Internal Medicine | 1964

Geophagia With Iron Deficiency And Hypokalemia: Cachexia Africana

Charles E. Mengel; William A. Carter; Edward S. Horton


Blood | 1968

Production of in vitro lytic characteristics of paroxysmal nocturnal hemoglobinuria erythrocytes in normal erythrocytes.

Herbert E. Kann; Charles E. Mengel; Wilhelm D. Meriwether; Larry Ebbert

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Bert W. O'Malley

Baylor College of Medicine

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