title: Comparative study of the protective effect between deferoxamine and deferiprone on chronic iron overload induced cardiotoxicity in rats.
abstract: Patients with iron overload frequently suffer from hemochromatosis of major organs, such as the heart and liver. Heart affection is the most common cause of death in patients with iron overload. Although the beneficial effects of deferoxamine (DFO) on iron-associated mortality are well documented, the role of deferiprone in the management of transfusional iron overload is controversial. The aim of this study was to compare the protective effect of iron chelators (DFO and deferiprone) individually and in combination with the anti-oxidant (vitamin C) in the prevention of myocardial damage. Sixty albino rats were divided into six groups: two control groups (noniron-loaded and iron-loaded) and four iron-loaded groups classified as follows: DFO group, DFO combined with vitamin C group, deferiprone group and deferiprone combined with vitamin C group. Heart tissue and blood samples were taken for histopathological examination of the heart, determination of total iron-binding capacity, 8-OH-deoxyguanosine (8-OH-dG), myocardial lipid peroxidation and glutathione (GSH) content. Less histopathological cardiac changes and a significant decrease in all biochemical parameters, except myocardial GSH, were observed in the deferiprone group. The addition of vitamin C improves the biochemical and histopathological changes in comparison to those rats administered DFO or deferiprone individually.
authors.affiliation: Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Tanta University, Egypt. ashlo2003@yahoo.com.au
authors.forename: A M
authors.initials: AM
authors.lastname: Emara
authors.forename: R S
authors.initials: RS
authors.lastname: El Kelany
authors.forename: K A
authors.initials: KA
authors.lastname: Moustafa
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use; D000077543:Deferiprone; D003676:Deferoxamine / Q000494:pharmacology* / Q000627:therapeutic use; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D006331:Heart Diseases / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D007501:Iron / Q000097:blood; D007502:Iron Chelating Agents / Q000494:pharmacology* / Q000627:therapeutic use; D019190:Iron Overload / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure; D011728:Pyridones / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D007502:Iron Chelating Agents; D011728:Pyridones; D017392:Thiobarbituric Acid Reactive Substances; D000077543:Deferiprone; D000080242:8-Hydroxy-2'-Deoxyguanosine; D007501:Iron; D003849:Deoxyguanosine; D005978:Glutathione; D003676:Deferoxamine; D001205:Ascorbic Acid