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Model Studies of the Iron-Catalysed Haber-Weiss Cycle and the Ascorbate-Driven Fenton Reaction
Abstract
Complementary hydroxylation assays and stopped-flow e.s.r. techniques have been employed in the investigation of the effect of various iron chelators (of chemical, biological and clinical importance) on hydroxyl-radical generation via the Haber-Weiss cycle and the ascorbate-driven Fenton reaction. Chelators have been identified which selectively promote or inhibit various reactions involved in hydroxyl-radical generation (for example, NTA and EDTA promote all the reactions of both the Haber-Weiss cycle and the ascorbate-driven Fenton reaction, whereas DTPA and phytate inhibit the recycling of iron in these reactions). The biological chelators succinate and citrate are shown to be relatively poor catalysts of the Haber-Weiss cycle, whereas they are found to be effective catalysts of .OH generation in the ascorbate-driven Fenton reaction. It is also suggested that continuous redox-cycling reactions between iron, oxygen and ascorbate may represent an important mechanism of cell death in biological systems.
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Cites
Iron-catalyzed hydroxyl radical formation. Stringent requirement for free iron coordination site.
Graf, E., Mahoney, J. R., Bryant, R. G., & Eaton, J. W. (1984) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)43139-5 · Cited by 855
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Metadata
- Authors
- Burkitt, M. J., & Gilbert, B. C.
- Venue
- Free Radical Research Communications
- Publisher
- Informa UK Limited
- Published
- 1990-01
- Volume
- 10
- Issue
- 4-5
- Pages
- 265-280
- ISSN
- 8755-0199 (ISSN-L)
- OpenAlex
- W2099229982
- Cited by
- 161
- References
- 1
- FWCI
- 5.91
- Type
- journal article
- Language
- en
- Open access
- closed
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- Burkitt, M. J., & Gilbert, B. C. (1990). Model Studies of the Iron-Catalysed Haber-Weiss Cycle and the Ascorbate-Driven Fenton Reaction. Free Radical Research Communications. https://doi.org/10.3109/10715769009149895
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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