The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Mitochondria as a source of reactive oxygen species during reductive stress in rat hepatocytes
Abstract
Cell killing, oxygen consumption, and hydroperoxide formation were determined in rat hepatocytes after glycolytic and respiratory inhibition. These conditions model the ATP depletion and reductive stress of anoxia (“chemical hypoxia”). Glycolysis was inhibited with iodoacetate, and mitochondrial electron transfer was blocked with sodium azide, cyanide, or myxothiazol. Cell killing, hydroperoxide formation, and inhibitor-insensitive oxygen consumption were greater after azide than after myxothiazol or cyanide. Desferrioxamine, an inhibitor of iron-catalyzed hydroxyl radical formation, delayed cell killing after each of the respiratory inhibitors. Anoxia also delayed cell killing during chemical hypoxia. However, during anoxic incubations, desferrioxamine did not delay the onset of cell death. These findings indicate that reactive oxygen species participate in lethal cell injury during chemical hypoxia. In isolated mitochondria, previous studies have shown that myxothiazol inhibits Q cycle-mediated ubisemiquinone formation in complex III (ubiquinol-cytochrome c oxidoreductase) and that ubisemiquinone can react with molecular oxygen to form superoxide. Decreased killing of hepatocytes with myxothiazol compared with azide suggests, therefore, that mitochondrial oxygen radical formation by complex III is involved in cell killing during reductive stress. In support of this hypothesis, myxothiazol reduced rates of cell killing and hydroperoxide formation in hepatocytes incubated with azide or cyanide. This mitochondrial mechanism for oxygen radical formation may be important in relative but not absolute hypoxia.
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Cites
Oxygen-Derived Free Radicals in Postischemic Tissue Injury
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Generation of superoxide anion by the NADH dehydrogenase of bovine heart mitochondria
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Ubisemiquinone is the electron donor for superoxide formation by complex III of heart mitochondria
Turrens, J. F., Alexandre, A., & Lehninger, A. L. (1985) · Archives of Biochemistry and Biophysics · doi:10.1016/0003-9861(85)90293-0 · Cited by 1,214
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Self-citationJaeschke, H., & Mitchell, J. R. (1989) · Biochemical and Biophysical Research Communications · doi:10.1016/0006-291x(89)91632-x · Cited by 188
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Self-citationMarotto, M. E., Thurman, R. G., & Lemasters, J. J. (1988) · Hepatology · doi:10.1002/hep.1840080325 · Cited by 135
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Cited by
Ischemic Cell Death in Brain Neurons
Lipton, P. (1999) · Physiological Reviews · doi:10.1152/physrev.1999.79.4.1431 · Cited by 3,043
Production of Reactive Oxygen Species by Mitochondria
Chen, Q., Vazquez, E. J., Moghaddas, S., Hoppel, C. L., & Lesnefsky, E. J. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m304854200 · Cited by 1,616
Selective degradation of mitochondria by mitophagy
Kim, I., Rodriguez-Enriquez, S., & Lemasters, J. J. (2007) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2007.03.034 · Cited by 1,558
Self-citationLemasters, J. J., Nieminen, A.-L., Qian, T., Trost, L. C., Elmore, S. P., Nishimura, Y., Crowe, R. A., Cascio, W. E., Bradham, C. A., Brenner, D. A., et al. (1998) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/s0005-2728(98)00112-1 · Cited by 1,387
Self-citationVanden Hoek, T. L., Becker, L. B., Shao, Z., Li, C., & Schumacker, P. T. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.29.18092 · Cited by 721
Metadata
- Authors
- Dawson, T. L., Gores, G. J., Nieminen, A. L., Herman, B., & Lemasters, J. J.
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 1993-04-01
- Volume
- 264
- Issue
- 4
- Pages
- C961-C967
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W2308938068
- Cited by
- 346
- References
- 10
- FWCI
- 4.12
- Type
- journal article
- Language
- en
- Open access
- closed
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- Dawson, T. L., Gores, G. J., Nieminen, A. L., Herman, B., & Lemasters, J. J. (1993). Mitochondria as a source of reactive oxygen species during reductive stress in rat hepatocytes. American Journal of Physiology-Cell Physiology. https://doi.org/10.1152/ajpcell.1993.264.4.c961
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