title: The iron paradox of heart and lungs and its implications for acute lung injury.
abstract: Iron is an essential requirement for the growth, development, and long term survival of most aerobic organisms. When control over safe iron sequestration is lost or compromised, leading to the release of low molecular mass forms of iron, the heart appears to be particularly sensitive to iron toxicity with cardiomyopathies often developing as a consequence. Iron toxicity, leading to iron-overload, is often treated in humans with the iron chelator desferrioxamine mesylate. Such treatment regimens designed to protect the heart can, however, often lead to lung injury and, in fact, several compounds with known iron chelating properties can induce severe lung dysfunction and injury. Based on these clinical observations and our recent laboratory data, we propose that the lungs actively accumulate reactive forms of iron for use in cellular growth and proliferation, and for the oxidative destruction of microbes, whereas the heart responds in the opposite way by actively removing iron which it finds extremely toxic.
authors.affiliation: Oxygen Chemistry Laboratory, Directorate of Anaesthesia and Critical Care, Royal Brompton and Harefield NHS Trust, Sydney Street, London, SW3 6NP, UK.
authors.forename: J M
authors.initials: JM
authors.lastname: Gutteridge
authors.forename: G J
authors.initials: GJ
authors.lastname: Quinlan
authors.forename: T W
authors.initials: TW
authors.lastname: Evans
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D019446:Endotoxemia / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007501:Iron / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress; D011990:Receptors, Transferrin / Q000378:metabolism; D012128:Respiratory Distress Syndrome / Q000378:metabolism* / Q000503:physiopathology*
chemical_list: D000975:Antioxidants; D011990:Receptors, Transferrin; D007501:Iron