title: Spondias pinnata stem bark extract lessens iron overloaded liver toxicity due to hemosiderosis in Swiss albino mice.
abstract: The present study was designed to evaluate the ameliorating effect of 70% methanol extract of Spondias pinnata (SPME) on iron overload induced liver injury. Iron overload was induced by intraperitoneal administration of iron-dextran into mice and resulting liver damage was manifested by significant rise in serum enzyme markers (ALT, AST, ALP and bilirubin) and reduction in liver antioxidants (SOD, CAT, GST and GSH). Hepatic iron, serum ferritin, lipid peroxidation, protein carbonyl and hydroxyproline contents were measured in response to the oral administration of SPME of different doses (50, 100 and 200 mg/kg body weight). In order to determine the efficiency as iron chelating drug, the release of iron from ferritin by SPME was further studied. Enhanced levels of antioxidant enzymes were detected in SPME treated mice. SPME produced a dose dependent inhibition of lipid peroxidation, protein oxidation, liver fibrosis; and levels of serum enzyme markers and ferritin were also reduced dose dependently. The liver iron content was also found to be less in SPME treated group compared to control group. The reductive release of ferritin iron was augmented significantly after dose dependent addition of SPME. The ameliorating effect of SPME on damaged liver was furthermore supported by the histopathological studies that showed improved histological appearances. In conclusion, the present results demonstrate the hepatoprotective efficiency of SPME in iron intoxicated mice, and hence possibly useful as iron chelating drug for iron overload diseases.
authors.affiliation: Division of Molecular Medicine, Bose Institute, P-1/12 CIT Scheme VIIM, Kolkata-700054, India.
authors.forename: Bibhabasu
authors.initials: B
authors.lastname: Hazra
authors.forename: Rhitajit
authors.initials: R
authors.lastname: Sarkar
authors.forename: Nripendranath
authors.initials: N
authors.lastname: Mandal
mesh_terms: D027926:Anacardiaceae / Q000737:chemistry*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy*; D005293:Ferritins / Q000097:blood; D005419:Flavonoids / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006397:Hematinics; D006486:Hemosiderosis / Q000139:chemically induced / Q000188:drug therapy*; D007501:Iron / Q000378:metabolism; D007505:Iron-Dextran Complex; D015227:Lipid Peroxidation / Q000187:drug effects; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D010636:Phenols / Q000627:therapeutic use*; D024301:Plant Bark / Q000737:chemistry; D010936:Plant Extracts / Q000627:therapeutic use*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D005419:Flavonoids; D006397:Hematinics; D008054:Lipid Peroxides; D010636:Phenols; D010936:Plant Extracts; D007505:Iron-Dextran Complex; D005293:Ferritins; D007501:Iron; D002374:Catalase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D005978:Glutathione