Health & Environmental Research Online (HERO)


Print Feedback Export to File
2498 
Journal Article 
An ultrastructural study of carbon disulphide induced liver injury in the rat 
Butler, WH; Chandra, SV; Magos, L 
1974 
Yes 
Journal of Pathology
ISSN: 0022-3417
EISSN: 1096-9896 
NIOSH/00127786 
112 
3 
147-158 
English 
4835118 
WOS:A1974T116200003 
An ultrastructural study of sodium-phenobarbital (57307) (BDH) mediated, carbon-disulphide (75150) (CS2) induced hepatic centrilobular hydropic degeneration was made in rats. Fasted male albino-Porton-rats were injected intraperitoneally with 80 milligrams per kilogram (mg/kg) BDH, followed 6 hours later with 50mg/kg BDH. The following day, rats were exposed to 4 milligrams per liter CS2 for 4 hours. Livers were removed 0, 1, 6, 12, 24, 36, and 48 hours after exposure and prepared for electron microscopy. CS2 alone produced no significant changes. BDH alone caused a proliferation of smooth endoplasmic reticulum (SER), particularly in the centrilobular cells. Animals killed immediately after combined treatment showed SER effects similar to BDH alone, along with slight dilatation of the rough endoplasmic reticulum (REF) and detachment of ribosomes. After 1 hour, creasing vesiculation of the RER and disaggregation of the ribosomes were seen. After 6 hours, the centrilobular parenchymal cells showed dilatation of the cytoplasmic cisternae, blebbing of nuclear membranes, and continuity between vesicular and extracellular spaces. The same changes were seen at 12 hours but to a greater degree. After 24 hours, vesicular membranes were discontinuous and fragmented and could not be characterized as from SER or RER. Nuclei contained one or more large nucleoli. At 36 hours, the number of parenchymal cells showing vesicular cytoplasm were reduced, confined to the centrilobular area, and contained large multiple autophagic vacuoles. After 48 hours, only parenchymal cells in the vicinity of the central vein still showed vesiculation of the endoplasmic reticulum cisternae. The most prominent feature was large autophagic vacuoles. The authors conclude that the reversible changes seen in the liver are due to damage to the phenobarbital induced SER.