Abstract
Redox cycling of catecholestrogen metabolites between quinone and catechol forms is a mechanism of generating potentially mutagenic oxygen radicals in estrogen-induced carcinogenesis. Consistent with this concept, multiple forms of oxygen radical-generated DNA damage are induced by estrogen in cell-free systems, in cells in culture and in rodents prone to estrogen-induced cancer. Metal ions, specifically iron, are necessary for the production of hydroxy radicals. Iron has not received much attention in discussions of estrogen-induced carcinogenesis and human hormone-associated cancer, and is the focus of this review. An elevated dietary iron intake enhances the incidence of carcinogen-induced mammary cancer in rats and estrogen-induced kidney tumors in Syrian hamsters. Estrogen administration increases iron accumulation in hamsters and facilitates iron uptake by cells in culture. In humans, elevated body iron storage has been shown to increase the risk of several cancers including breast cancer. A role of iron in hormone-associated cancer in humans offers attractive routes for cancer prevention by regulating metal ion metabolism and interfering with iron accumulation in tissues.
Keywords: Estrogen-Induced Cancer, Lipid Hydroperoxides
Current Medicinal Chemistry
Title: Role of Iron in Estrogen-Induced Cancer
Volume: 8 Issue: 7
Author(s): Joachim G. Liehr and J. Shawn Jones
Affiliation:
Keywords: Estrogen-Induced Cancer, Lipid Hydroperoxides
Abstract: Redox cycling of catecholestrogen metabolites between quinone and catechol forms is a mechanism of generating potentially mutagenic oxygen radicals in estrogen-induced carcinogenesis. Consistent with this concept, multiple forms of oxygen radical-generated DNA damage are induced by estrogen in cell-free systems, in cells in culture and in rodents prone to estrogen-induced cancer. Metal ions, specifically iron, are necessary for the production of hydroxy radicals. Iron has not received much attention in discussions of estrogen-induced carcinogenesis and human hormone-associated cancer, and is the focus of this review. An elevated dietary iron intake enhances the incidence of carcinogen-induced mammary cancer in rats and estrogen-induced kidney tumors in Syrian hamsters. Estrogen administration increases iron accumulation in hamsters and facilitates iron uptake by cells in culture. In humans, elevated body iron storage has been shown to increase the risk of several cancers including breast cancer. A role of iron in hormone-associated cancer in humans offers attractive routes for cancer prevention by regulating metal ion metabolism and interfering with iron accumulation in tissues.
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Cite this article as:
Liehr G. Joachim and Jones Shawn J., Role of Iron in Estrogen-Induced Cancer, Current Medicinal Chemistry 2001; 8 (7) . https://dx.doi.org/10.2174/0929867013372931
DOI https://dx.doi.org/10.2174/0929867013372931 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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