Journal of Lipid Research, Vol 23, 667-679, Copyright © 1982 by Lipid Research, Inc.
Alterations in lipoprotein composition associated with galactosamine- induced rat liver injury
CK Cartwright, JB Ragland, SW Weidman and SM Sabesin
The apoprotein and lipid composition and the morphology of lipoproteins was
determined in rats with D-(+)-galactosamine (GalN) hepatitis. Single
intraperitoneal injections of GalN at several dose levels and postinjection
exsanguination times resulted in depressed levels of cholesteryl esters, an
index of plasma lecithin:cholesterol acyltransferase (LCAT) activity, and
increased levels of phospholipids, unesterified cholesterol, and
triglycerides. Plasma withdrawn from rats 24 hr after injection of 1000
mg/kg GalN was most deficient in cholesteryl ester and was studied further
by sequential isolation of VLDL, LDL, HDL1, HDL2, and HDL3. The increased
plasma triglyceride (TG) after GalN treatment accumulated in TG-rich VLDL
which contained two types of particles: a large (mean diameter 193.6 +/-
48.3 nm) and rough- edged particle, and a smooth one with a mean diameter
(63.4 +/- 13.2 nm) similar to control VLDL (69.4 +/- 20.2 nm). The
increased phospholiThe increased plasma triglyceride (TG) after GalN
treatment accumulated in TG-rich VLDL which contained two types of
particles: a large (mean diameter 193.6 +/- 48.3 nm) and rough-edged
particle, and a smooth one with a mean diameter (63.4 +/- 13.2 nm) similar
to control VLDL (69.4 +/- 20.2 nm). The increased phospholiThe increased
plasma triglyceride (TG) after GalN treatment accumulated in TG-rich VLDL
which contained two types of particles: a large (mean diameter 193.6 +/-
48.3 nm) and rough-edged particle, and a smooth one with a mean diameter
(63.4 +/- 13.2 nm) similar to control VLDL (69.4 +/- 20.2 nm). The
increased phospholipids and unesterified cholesterol were predominantly in
LDL, HDL1, and HDL2 which were largely rouleaux of flattened vesicles.
Density gradient ultracentrifugation of d greater than 1.006 g/ml
lipoproteins confirmed these results. GalN hepatitis appeared to decrease
the larger apoB335K subspecies and the apoC-III0 and apoC-III2 content of
VLDL. However, total apoB concentration as GalN VLDL was increased 2.6-fold
over control. LDL and HDL were markedly enriched in apoE. LDL apoB
concentration was decreased by 41% while HDL was deficient in apoA-I, A-II
and A-IV, and C. These results demonstrate association of increased plasma
triglycerides with particles of grossly abnormal apoprotein composition,
and the association of increased plasma phospholipids and unesterified
cholesterol with apoE-rich lipoproteins during the LCAT defect produced by
GalN hepatitis. These abnormal lipoproteins may represent an abnormal level
of normal LCAT substrates important in the transport and esterification of
plasma cholesterol.
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