Treatment with the Iron Chelator, Deferoxamine Mesylate, Alters Serum Markers of Oxidative Stress in Stroke Patients
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ORIGINAL ARTICLE
Treatment with the Iron Chelator, Deferoxamine Mesylate, Alters Serum Markers of Oxidative Stress in Stroke Patients Magdy Selim
Received: 21 September 2009 / Accepted: 6 October 2009 / Published online: 10 December 2009 # Springer Science+Business Media, LLC 2009
Abstract The iron chelator, deferoxamine mesylate (DFO), has shown neuroprotective effects, mediated via suppression of iron-induced hydroxyl radical formation, in various animal models of ischemic and hemorrhagic stroke. Therefore, the objective of this study was to investigate whether DFO can exert similar actions in stroke patients, by examining the effects of treatment with DFO on biological markers of oxidative stress, namely serum total hydroperoxides and lipoperoxides and total radical trapping antioxidant capacity (TRAP), in stroke patients. We found that serum levels of peroxides were reduced, and TRAP levels increased after a 3-day treatment with DFO (500 mg). These findings provide a preliminary proof of concept that DFO can exert potential antioxidant neuroprotective effects in stroke patients. Future, larger-scale, randomized, and controlled studies to further evaluate the safety and efficacy of DFO in patients with stroke are warranted. Keywords Deferoxamine . Iron . Stroke . Oxidative stress
Introduction Accumulating evidence indicates that neuronal damage following stroke is partly linked to disturbances of iron homeostasis and iron-mediated neurotoxicity [1–3]. Enhanced deposition of iron is seen in the rat brain after transient ischemia, and the timing and sites of new iron deposition correlate with late neuronal death and lipid peroxidation
[1, 2]. Iron is also implicated in secondary neuronal injury after hemorrhagic stroke [4, 5]. Transitional iron induces neuronal injury by catalyzing Haber–Weiss reaction, in which superoxide and hydrogen peroxide are converted into highly reactive toxic hydroxyl radicals [6, 7]. Increased hydroxyl radical formation leads to oxidative stress and subsequent cell death. These links between iron and the pathogenesis of neuronal damage after stroke provide a rationale for therapeutic use of iron-modifying agents to prevent or arrest the progression of neuronal loss in stroke patients. Deferoxamine mesylate (DFO) forms a stable complex with ferric iron, thus decreasing its availability for the production of hydroxyl radicals, and has shown neuroprotective effects, mediated via suppression of iron-induced hydroxyl radical formation, in various animal models of ischemic and hemorrhagic stroke [8–14]. However, it is unknown if DFO has similar neuroprotective effects in stroke patients. The objective of this study was to examine the effects of DFO on biological markers of oxidative stress, namely serum total hydroperoxides and lipoperoxides and total radical trapping antioxidant capacity (TRAP), in stroke patients [15, 16]. Elucidating that DFO can exert potential neuroprotective effects, by suppressing markers of oxidative stress or activating antioxidant capacity, in stroke patients is i
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