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1.
Biometals ; 18(6): 567-75, 2005 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-16388396

RESUMEN

Iron overload aggravates tissue damage caused by ischemia and ethanol intoxication. The underlying mechanisms of this phenomenon are not yet clear. To clarify these mechanisms we followed free iron ("loosely" bound redox-active iron) concentration in livers from rats subjected to experimental iron overload, acute ethanol intoxication, and ex vivo warm ischemia. The levels of free iron in non-homogenized liver tissues, liver homogenates, and hepatocyte cultures were analyzed by means of EPR spectroscopy. Ischemia gradually increased the levels of endogenous free iron in liver tissues and in liver homogenates. The increase was accompanied by the accumulation of lipid peroxidation products. Iron overload alone, known to increase significantly the total tissue iron, did not affect either free iron levels or lipid peroxidation. Homogenization of iron-loaded livers, however, resulted in the release of a significant portion of free iron from endogenous depositories. Acute ethanol intoxication increased free iron levels in liver tissue and diminished the portion of free iron releasing during homogenization. Similarly to liver tissue, the primary hepatocyte culture loaded with iron in vitro released significantly more free iron during homogenization compared to non iron-loaded hepatocyte culture. Analyzing three possible sources of free iron release under these experimental conditions in liver cells, namely ferritin, intracellular transferrin-receptor complex and heme oxygenase, we suggest that redox active free iron is released from ferritin under ischemic conditions whereas ethanol and homogenization facilitate the release of iron from endosomes containing transferrin-receptor complexes.


Asunto(s)
Etanol/administración & dosificación , Sobrecarga de Hierro/metabolismo , Hierro/metabolismo , Isquemia/metabolismo , Animales , Células Cultivadas , Dieta , Modelos Animales de Enfermedad , Espectroscopía de Resonancia por Spin del Electrón , Femenino , Hepatocitos/metabolismo , Hepatocitos/patología , Inyecciones Intraperitoneales , Sobrecarga de Hierro/patología , Isquemia/patología , Hígado/irrigación sanguínea , Hígado/metabolismo , Hígado/patología , Ratas , Ratas Wistar
2.
J Bioenerg Biomembr ; 34(1): 67-79, 2002 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-11860182

RESUMEN

Hepatic fibrosis due to iron overload is mediated by oxidant stress. The basic mechanisms underlying this process in vivo are still little understood. Acutely iron-dosed gerbils were assayed for lobular accumulation of hepatic lipid peroxidation by-products, oxidant-stress gene response, mitochondrial energy-dependent functions, and fibrogenesis. Iron overload in nonparenchymal cells caused an activation of hepatic stellate cells and fibrogenesis. Oxidant-stress gene response and accumulation of malondialdehyde-protein adducts were restricted to iron-filled nonparenchymal cells, sparing nearby hepatocytes. Concomitantly, a significant rise in the mitochondrial desferrioxamine-chelatable iron pool associated with the impairment of mitochondrial oxidative metabolism and the hepatic ATP decrease, was detected. Ultrastructural mitochondrial alterations were observed only in nonparenchymal cells. All biochemical and functional derangements were hindered by in vivo silybin administration which blocked completely fibrogenesis. Iron-induced oxidant stress in nonparenchymal cells appeared to bring about irreversible mitochondrial derangement associated with the onset of hepatic fibrosis.


Asunto(s)
Hepatocitos/metabolismo , Hierro/toxicidad , Estrés Oxidativo/efectos de los fármacos , Adenosina Trifosfato/biosíntesis , Animales , Enfermedad Hepática Inducida por Sustancias y Drogas , Transporte de Electrón , Complejo IV de Transporte de Electrones/metabolismo , Fibrosis/inducido químicamente , Fibrosis/patología , Fibrosis/prevención & control , Gerbillinae , Hepatocitos/efectos de los fármacos , Hepatocitos/patología , Hierro/administración & dosificación , Sobrecarga de Hierro/complicaciones , Sobrecarga de Hierro/patología , Hepatopatías/patología , Hepatopatías/prevención & control , Masculino , Potenciales de la Membrana , Mitocondrias Hepáticas/efectos de los fármacos , Mitocondrias Hepáticas/metabolismo , Mitocondrias Hepáticas/patología , Enfermedades Mitocondriales/inducido químicamente , Enfermedades Mitocondriales/prevención & control , Estrés Oxidativo/fisiología , Silimarina/farmacología , Silimarina/uso terapéutico
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