Abstract
Desferrioxamine (DFO), deferiprone (DFP) and deferasirox (DFX) are promising effective iron chelators for the treatment of iron overload in b-thalassemia patients; nonetheless, their side effects have also been reported. 3-Hydroxypyridinone derivatives are being developed as a safer new chelator and in combined chelation therapy. We evaluated the iron-chelating activity of 1-(N-acetyl-6-aminohexyl)-3-hydroxypyridin-4-one (CM1) in iron-loaded C57BL6 mice. The feeding of a ferrocene-supplemented diet (Fe diet) to mice resulted in iron overload, detectable plasma nontransferrin-bound iron (NTBI) and labile plasma iron (LPI), and increases of red cell membrane iron, plasma malondialdehyde (MDA) and excessive tissue iron deposits. Like DFP, the CM1 lowered the levels of the membrane non-heme iron, the NTBI and LPI (p
Highlights
In iron overload, excessive amounts of iron catalyzes the production of reactive oxygen species (ROS) via HaberWeiss and Fenton reactions, and in turn the ROS can damage cells and tissues of the heart, liver, pancreas and endocrine glands, leading to dysfunctions of these vital organs [1]
The feeding of a ferrocene-supplemented diet (Fe diet) to mice resulted in iron overload, detectable plasma nontransferrin-bound iron (NTBI) and labile plasma iron (LPI), and increases of red cell membrane iron, plasma malondialdehyde (MDA) and excessive tissue iron deposits
Iron overload was induced by feeding the mice a normal chow diet (N diet) and the N diet supplemented with 0.2% (w/w) ferrocene (Fe diet) for 90 days [31]
Summary
Excessive amounts of iron catalyzes the production of reactive oxygen species (ROS) via HaberWeiss and Fenton reactions, and in turn the ROS can damage cells and tissues of the heart, liver, pancreas and endocrine glands, leading to dysfunctions of these vital organs [1]. Non-transferrin bound iron (NTBI) and labile plasma iron (LPI) appearing in the plasma of thalassemia patients with iron overload play a major role in many pathological conditions [2,3]. These two toxic forms of the iron seem to be translocated across cell membrane irregularly; they are susceptible to chelation outside the cells [4]. Levels of the NTBI, LPI and LIP have been proposed for the assessment of iron overload and evaluation of the efficiency in chelation therapy [6]. We investigated a potential role of our new chelator, CM1 in the treatment of iron-loaded mice
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