Most free-radical injury is iron-related: It is promoted by iron, hemin, holoferritin and vitamin c, and inhibited by desferoxamine and apoferritin
Article first published online: 1 JAN 1996
Copyright © 1994 AlphaMed Press
Volume 12, Issue 3, pages 289–303, 1994
How to Cite
Herbert, V., Shaw, S., Jayatilleke, E. and Stopler-Kasdan, T. (1994), Most free-radical injury is iron-related: It is promoted by iron, hemin, holoferritin and vitamin c, and inhibited by desferoxamine and apoferritin. STEM CELLS, 12: 289–303. doi: 10.1002/stem.5530120305
- Issue published online: 23 DEC 2008
- Article first published online: 1 JAN 1996
- Manuscript Received: 13 DEC 1993
- Manuscript Accepted: 13 DEC 1993
- Catalytic iron;
- Redox vitamin C;
- Iron proteins;
- Pro-tumor iron-ascorbate;
- Tumor-destroying iron-ascorbate
Iron is a double-edged sword. In moderate quantities and leashed to protein, it is an essential element in all cell metabolism and growth, but it is toxic when unleashed . Because of its ability to switch back and forth between ferrous and ferric oxidation states, iron is both a strong biological oxidant and reductant.
The human diet contains a multitude of natural chemicals which are carcinogens and anti-carcinogens, many of which act by generating oxygen radicals, which initiate degenerative processes related to cancer, heart disease and aging (the “oxygen radical hypothesis of aging”) . Among these many dietary chemicals are many redox agents, including vitamin C and beta carotene .
Free radical damage is produced primarily by the hydroxyl radical (·OH) [4, 5]. Most of the ·OH generated in vivo comes from iron-dependent reduction of H2O2 [4, 5]. Supporting too much iron as a free radical-generating culprit in the risk of cancer, NHANES I data indicated that high body iron stores, manifested by increased transferrin saturation, are associated with an increased cancer risk . Other data  shows an increased heart attack risk.