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In vivo assessment of microcystin-LR-induced hepatotoxicity in the rat using proton nuclear magnetic resonance (1H-NMR) imaging.
Sturgeon, S A; Towner, R A.
  • Sturgeon SA; North Queensland Magnetic Resonance Centre, Department of Physiology and Pharmacology, James Cook University, Townsville, Qld., Australia.
Biochim Biophys Acta ; 1454(3): 227-35, 1999 Aug 30.
Article en En | MEDLINE | ID: mdl-10452957
Microcystin-LR (MCLR)-induced hepatotoxicity was assessed in vivo in male Sprague-Dawley rats (150-350 g) using magnetic resonance imaging (MRI). Following the intraperitoneal administration of MCLR (LD(50)), a region of damage, characterised by increased signal intensity on T(2)-weighted images, was seen proximal to the hepatic portal vein in the liver. Similarly, increased signal intensity was seen in the chemical-shift selective images (CSSI) of water frequency, proximal to the hepatic portal vein in the liver. This indicates that the increased signal intensity observed in the T(2)-weighted images was due to an increased amount of magnetic resonance (MR) visible protons in the tissue which represents an oedematous response. Image analysis of regions of apparent damage around the hepatic portal vein indicated a statistically significant increase in signal intensity in this region. Mitochondrial swelling and lipid inclusions were observed by transmission electron microscopy (TEM) in samples obtained from the oedematous regions of the liver using spatial coordinates from the magnetic resonance (MR) images. Massive haemorrhagic necrosis and nuclear swelling were observed by light microscopy in the centrilobular regions of the lobules.
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Banco de datos: MEDLINE Asunto principal: Péptidos Cíclicos / Toxinas Bacterianas / Enfermedad Hepática Inducida por Sustancias y Drogas / Hígado Límite: Animals Idioma: En Año: 1999 Tipo del documento: Article
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Banco de datos: MEDLINE Asunto principal: Péptidos Cíclicos / Toxinas Bacterianas / Enfermedad Hepática Inducida por Sustancias y Drogas / Hígado Límite: Animals Idioma: En Año: 1999 Tipo del documento: Article