Most free‐radical injury is iron‐related: It is promoted by iron, hemin, holoferritin and vitamin c, and inhibited by desferoxamine and apoferritin

Abstract

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 [1]. 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”) [2]. Among these many dietary chemicals are many redox agents, including vitamin C and beta carotene [3]. 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 [6]. Other data [1] shows an increased heart attack risk.