Fenton and Haber-Weiss reactions are a source of oxidative stress. The generation of oxygen free radicals occurs first with the reduction of ferric to ferrous iron and then by the Fenton reaction with ferrous iron catalyzing the breakdown of hydrogen peroxide to hydroxyl radical and hydroxyl. The net reaction is termed the Haber-Weiss reaction.

Fenton and Haber-Weiss reactions are a source of oxidative stress. The generation of oxygen free radicals occurs first with the reduction of ferric to ferrous iron and then by the Fenton reaction with ferrous iron catalyzing the breakdown of hydrogen peroxide to hydroxyl radical and hydroxyl. The net reaction is termed the Haber-Weiss reaction.

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Iron homeostasis is often disrupted in acute disease with an increase in catalytic free iron leading to the formation of reactive oxygen species and subsequent tissue-specific oxidative damage. This article highlights the potential therapeutic benefit of exogenous hepcidin to prevent and treat iron-induced injury, specifically in the management of...

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... iron (CFI) is undetectable and plasma iron is tightly bound to TF. CFI, which can be thought of as unbound iron, is a promiscuous molecule that functions as a "bad-actor." When CFI is in its ferrous state (Fe 21 ), CFI can initiate the Fenton reactions or when iron is unbound in its ferric state (Fe 31 ) CFI can initiate Haber-Weiss reactions (Fig. 2). These reactions generate oxygen free radicals, such as hydroxyl radical (OH À ), peroxynitrite (ONOO À ), superoxide free radical anion (O 2 À ), and hydrogen peroxide (H 2 O 2 ). 23,24 These oxygen free radicals are often referred to as reactive oxygen species (ROS) and can damage important macromolecules. ROS have been shown to ...

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... Human physiologic systems have evolved to orchestrate a careful balance of iron binding and release that enables us to avoid injury while effectively delivering this essential nutrient to tissues. In acute illnesses, however, iron homeostasis is often disrupted and ferrous iron is produced, which contributes to tissue injury, as well as to a higher risk of bacterial infection (44,45). Many investigations, based in clinical and laboratory settings, have shown that iron supplementation causes more severe infections of Mycobacterium tuberculosis (46) but lower virulence of the enteric pathogen Citrobacter (47). ...
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... This is in line with experimental studies in murine models where the data show that hepcidin-induced hypoferremia can act as a defence mechanism against bacterial infection 22,[51][52][53][54] . Administration of exogenous hepcidin has been suggested to be of therapeutic value in selected cases of hyperferremia 55 . High iron concentrations have been reported to increase the lethal effects of siderophile bacteria in vivo and also in fungal infections and the reduction of available plasma iron is most likely beneficial for the host unless prolonged and leading to anaemia 51,55,56 . ...
... Administration of exogenous hepcidin has been suggested to be of therapeutic value in selected cases of hyperferremia 55 . High iron concentrations have been reported to increase the lethal effects of siderophile bacteria in vivo and also in fungal infections and the reduction of available plasma iron is most likely beneficial for the host unless prolonged and leading to anaemia 51,55,56 . ...
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... Iron is an essential nutrient for both humans under physiological conditions and for pathogenic bacteria during infection [1][2][3]. Strict regulation of iron homeostasis in humans under both physiological and pathological conditions is essential [1,3,4]. Under normal physiological conditions, iron is mainly stored intracellularly in erythrocytes, or is bound in the plasma to transferrin, which has a high affinity for ferric iron (Fe 3+ ) [1,3]. ...
... Following an insult, such as an infection, iron homeostasis is disrupted, and nutritional immunity is enhanced [1,4]. Nutritional immunity is a vertebrate strategy to restrict the availability of essential nutrients, including iron, to invading pathogens [1,2,5,6]. ...
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AKI remains a major public health concern. Despite years of investigation, no intervention has been demonstrated to reliably prevent AKI in humans. Thus, development of novel therapeutic targets is urgently needed. An important role of iron in the pathophysiology of AKI has been recognized for over three decades. When present in excess and in nonphysiologic labile forms, iron is toxic to the kidneys and multiple other organs, whereas iron chelation is protective across a broad spectrum of insults. In humans, small studies have investigated iron chelation as a novel therapeutic strategy for prevention of AKI and extrarenal acute organ injury, and have demonstrated encouraging initial results. In this review, we examine the existing data on iron chelation for AKI prevention in both animal models and human studies. We discuss practical considerations for future clinical trials of AKI prevention using iron chelators, including selection of the ideal clinical setting, patient population, iron chelating agent, and dosing regimen. Finally, we compare the key differences among the currently available iron chelators, including pharmacokinetics, routes of administration, and adverse effects.