In vivo formation of H<sub>2</sub>O<sub>2</sub> in red cells during exposure to hyperoxia

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

doi:10.1172/JCI107029

¹Division of Hematology and Oncology, Department of Medicine, The University of Missouri, Columbia, Missouri 65201

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¹Division of Hematology and Oncology, Department of Medicine, The University of Missouri, Columbia, Missouri 65201

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¹Division of Hematology and Oncology, Department of Medicine, The University of Missouri, Columbia, Missouri 65201

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Published in Volume 51, Issue 8 on August 1, 1972
J Clin Invest. 1972;51(8):2211–2213. https://doi.org/10.1172/JCI107029.
© 1972 The American Society for Clinical Investigation

Published August 1, 1972 - Version history

Chow-fed and tocopherol-deficient mice were given aminotriazole (AT), exposed to 100% O₂ 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 H₂O₂. 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 H₂O₂ 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 H₂O₂.

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