Reactive oxygen species are involved in the aging process and diseases. Despite the important role of Cu/Zn SOD (superoxide dismutase) encoded by SOD1, SOD1−/− mice appear to grow normally under conventional breeding conditions. In the present paper we report on a novel finding showing a distinct connection between oxidative stress in erythrocytes and the production of autoantibodies against erythrocytes in SOD1−/− mice. Evidence is presented to show that SOD1 is primarily required for maintaining erythrocyte lifespan by suppressing oxidative stress. A SOD1 deficiency led to an increased erythrocyte vulnerability by the oxidative modification of proteins and lipids, resulting in anaemia and compensatory activation of erythropoiesis. The continuous destruction of oxidized erythrocytes appears to induce the formation of autoantibodies against certain erythrocyte components, e.g. carbonic anhydrase II, and the immune complex is deposited in the glomeruli. The administration of an antioxidant, N-acetylcysteine, suppressed erythrocyte oxidation, ameliorated the anaemia, and inhibited the production of autoantibodies. These data imply that a high level of oxidative stress in erythrocytes increases the production of autoantibodies, possibly leading to an autoimmune response, and that the intake of antioxidants would prevent certain autoimmune responses by maintaining an appropriate redox balance in erythrocytes.
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Research Article|
February 12 2007
Elevated oxidative stress in erythrocytes due to a SOD1 deficiency causes anaemia and triggers autoantibody production
Yoshihito Iuchi;
Yoshihito Iuchi
*Department of Biomolecular Function, Graduate School of Medical Science, Yamagata University, Yamagata, Japan
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Futoshi Okada;
Futoshi Okada
*Department of Biomolecular Function, Graduate School of Medical Science, Yamagata University, Yamagata, Japan
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Kunishige Onuma;
Kunishige Onuma
*Department of Biomolecular Function, Graduate School of Medical Science, Yamagata University, Yamagata, Japan
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Tadashi Onoda;
Tadashi Onoda
†Department of Immunology, Yamagata University School of Medicine, Yamagata, Japan
‡Department of Paediatrics, Yamagata University School of Medicine, Yamagata, Japan
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Hironobu Asao;
Hironobu Asao
†Department of Immunology, Yamagata University School of Medicine, Yamagata, Japan
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Masanobu Kobayashi;
Masanobu Kobayashi
§Division of Cancer Pathobiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan
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Junichi Fujii
Junichi Fujii
1
*Department of Biomolecular Function, Graduate School of Medical Science, Yamagata University, Yamagata, Japan
1To whom correspondence should be addressed (email [email protected]).
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Publisher: Portland Press Ltd
Received:
September 08 2006
Revision Received:
October 23 2006
Accepted:
October 24 2006
Accepted Manuscript online:
October 24 2006
Online ISSN: 1470-8728
Print ISSN: 0264-6021
The Biochemical Society, London
2007
Biochem J (2007) 402 (2): 219–227.
Article history
Received:
September 08 2006
Revision Received:
October 23 2006
Accepted:
October 24 2006
Accepted Manuscript online:
October 24 2006
Citation
Yoshihito Iuchi, Futoshi Okada, Kunishige Onuma, Tadashi Onoda, Hironobu Asao, Masanobu Kobayashi, Junichi Fujii; Elevated oxidative stress in erythrocytes due to a SOD1 deficiency causes anaemia and triggers autoantibody production. Biochem J 1 March 2007; 402 (2): 219–227. doi: https://doi.org/10.1042/BJ20061386
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