Journal of The Showa Medical Association
Online ISSN : 2185-0976
Print ISSN : 0037-4342
ISSN-L : 0037-4342
CHANGE OF SERUM LIPOPROTEIN ASSOCIATED WITH CARBON TETRACHLORIDE-INDUCED CHRONIC LIVER INJURY IN RATS
Sadao NAKAYAMAAkihiko YURAShunsuke IMASAKAHideyuki KURISHIMAMakoto MAYANAGIAmi MANABEKatsuji OGUCHI
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1991 Volume 51 Issue 2 Pages 172-178

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Abstract
We investigated changes of serum lipoproteins and pathological observations of the liver in rats with chronic liver injury induced by carbon tetrachloride (CCl4) . Male, Sprague-Dawley, 6 week old, 150-170g rats were used in the experiment. CCl4 was dissolved in olive oil, and 2 ml/kg body weight was given to each animal. Chronic liver injury was produced in rats by oral administration of 0.5 ml/kg CCl4 twice weekly for 10 weeks. Rats were sacrificed after 5 (5W-CCl4) and 10 (10W-CCl4) weeks of CCl4 administration, and the serum and livers were collected. In the 5W-CCl4 group, these was increase of high density lipoprotein subfractions (HDL1, HDL2, HDL3) and low density lipoprotein (LDL) . Increased HDL1 and LDL, and decreased very low density lipoprotein (VLDL) were also evident in the 10W-CCl4 group. The lipid content in HDL and LDL fractions were increased by CCl4 and the total protein (TP) content was decreased in the HDL. Decrease of lipid and TP content in VLDL, were also evident in the 10W-CCl4 group. Increases of total cholesterol and triglyceride, and decrease of phospholipid (PL) in the liver were observed in the 5W-CCl4 group. PL in the liver was also decreased by 10W-CCl4. Pathological examination of the livers revealed that CCl4 caused the formation of septum and pseudolobules by the proliferation of connective tissue. Lipid deposition in the pseudolobule of the liver was caused by 5W-CCl4. Loss of cytoplasm and nuclei, vacuolation and necrosis in the pseudolobular hepatocytes, but no lipid deposition were caused by 10W-CCl4. The results suggest that the increase of HDL and LDL by 5W-CCl4 was due to damage of lipoprotein metablolism in the liver associated with liver injury, and decrease of VLDL and increase of HDL1 and LDL by 10W-CCl4 were due to defective lipoprotein metabolism, and lipoprotein formation.
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