Ultrastructural changes in hepatic sinusoidal endothelial cells acutely exposed to colloidal iron

• Published in: Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie Vol. 55; no. 1; pp. 11 - 16
• Main Authors: Bassett, Mark L., Dahlstrom, Jane E., Taylor, Matthew C., Koina, Mark E., Maxwell, Lesley, Francis, Douglas, Jain, Sanjiv, McLean, Allan J.
• Format: Journal Article
• Language: English
• Published: Jena Elsevier GmbH 2003; Elsevier
• Subjects: Animals; Biological and medical sciences; colloid; Colloids; Electron Probe Microanalysis; endothelial; Female; Hepatic; Injections, Intravenous; iron; Iron - analysis; Iron Compounds - administration & dosage; Iron Compounds - toxicity; Kupffer Cells - drug effects; Kupffer Cells - ultrastructure; Male; Maltose; Medical sciences; Microscopy, Electron; Microvilli - drug effects; Microvilli - ultrastructure; Rats; Rats, Wistar; sinusoidal; iron; colloid; Hepatic; sinusoidal; endothelial
• ISSN: 0940-2993; 1618-1433
• DOI: 10.1078/0940-2993-00296

Hepatic sinusoidal endothelial cells form an important interface between the vascular system, represented by the sinusoids, and the space of Disse that surrounds the hepatocyte microvilli. This study aimed to assess the light microscopic and ultrastructural effects of acute exposure of hepatic sinusoidal endothelial cells to colloidal iron by injection of rats with iron polymaltose. Eight minutes after a single intravenous injection of iron polymaltose sinusoidal endothelial cells showed defenestration, and thickening and layering as assessed by transmission electron microscopy. Kupffer cells and stellate cells appeared activated. These changes were not observed in control animals, experiments using equivalent doses of maltose, or experiments using colloidal carbon except for Kupffer cell activation due to colloidal carbon. No significant light microscopic changes were seen in study or control animals. The findings indicate that acute exposure to colloidal iron causes changes in hepatic sinusoidal endothelial cells, stellate cells and Kupffer cells. This may be the result of a direct toxic effect of iron or increased production of reactive oxygen species. These observations suggest a possible mechanism for defenestration of sinusoidal endothelial cells in ageing and in disease states.