Abstract
The flavonol rutin has been shown to possess antioxidant and iron chelating properties in vitro and in vivo. These dual properties are beneficial as therapeutic options to reduce iron accumulation and the generation of reactive oxygen species (ROS) resultant from excess free iron. The effect of rutin on iron metabolism has been limited to studies performed in wildtype mice either injected or fed high-iron diets. The effect of rutin on iron overload caused by genetic dysregulation of iron homoeostasis has not yet been investigated. In the present study we examined the effect of rutin treatment on tissue iron loading in a genetic mouse model of iron overload, which mirrors the iron loading associated with Type 3 hereditary haemochromatosis patients who have a defect in Transferrin Receptor 2 (TFR2). Male TFR2 knockout (KO) mice were administered rutin via oral gavage for 21 continuous days. Following treatment, iron levels in serum, liver, duodenum and spleen were assessed. In addition, hepatic ferritin protein levels were determined by Western blotting, and expression of iron homoeostasis genes by quantitative real-time PCR. Rutin treatment resulted in a significant reduction in hepatic ferritin protein expression and serum transferrin saturation. In addition, trends towards decreased iron levels in the liver and serum, and increased serum unsaturated iron binding capacity were observed. This is the first study to explore the utility of rutin as a potential iron chelator and therapeutic in an animal model of genetic iron overload.
Highlights
Iron is a fundamental micronutrient for all organisms; it is involved in several essential functions such as oxygen metabolism, electron transfer and in enzymes important for DNA and RNA synthesis [1]
We examined the Tfr2 KO mouse model of iron overload to determine whether oral administration of rutin can be used to rescue mice from iron overload typical of that seen in Type 3 HH patients
This analysis indicated that rutin treatment for 21 days did not significantly affect haematological parameters of the treated mice
Summary
Iron is a fundamental micronutrient for all organisms; it is involved in several essential functions such as oxygen metabolism, electron transfer and in enzymes important for DNA and RNA synthesis [1]. Iron dysregulation can result in numerous clinical disorders including anaemia and haemochromatosis. The flavonoid family of compounds have broad pharmacological activities and have been shown to be beneficial in numerous diseases including diabetes mellitus, allergy, cancer, viral infections, headache, stomach and duodenal ulcer, parodentosis and inflammation [4,5]. Pharmacological activities typical of flavonoids include interactions with enzymes, hormone carriers, DNA, antioxidant (free radical scavenging) and iron chelating properties [6,7,8,9]. The latter makes these compounds interesting options for the treatment of iron overload disorders
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