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Iron is an essential mineral required for many functions in animal physiology. The iron redox couple reaction mediates the transfer of single electrons through the reversible oxidation/reduction of Fe2+ and Fe3+. This redox cycling is useful for many metabolic pathways essential to life, such as cell cycle progression and division, oxygen transport, mitochondrial activity and immune system function. As a consequence of iron redox reactions, the same metabolic pathways generate reactive oxygen species (ROS) that provide the background for oxidative stress (ie, an imbalance between the production of free radicals and the ability of the body to counteract their harmful effects).
Iron homeostasis is finely tuned: if dysregulated, conditions of iron overload or iron deficiencies can occur. Iron deficiency effects go beyond the well-known importance of iron in the synthesis and function of haemoglobin and myoglobin (and subsequently oxygen transport), by also having further impact on the oxidative status of animals.
Iron is a cofactor of enzymes involved in the scavenging of ROS, namely catalase, peroxidase and superoxide dismutase (SOD)1. Therefore, iron deficiency reduces organism protection against oxidative stress. On the other hand, excess of iron may have similar effects: iron can bind to the Mn-SODs, with similar affinities and geometries as manganese,2,3 resulting in the inactivation …
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