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in lipopolysaccharide-induced hepatic
injury
Departments of 1 Internal Medicine and 3 Pathology, College of Medicine, University of Kentucky, and the 2 Lexington Veterans Affairs Medical Center, Lexington, Kentucky 40536
S-adenosylmethionine
(Adomet) is a substrate for de novo synthesis of choline. Adomet
deficiency occurs in certain types of liver injury, and the injury is
attenuated by exogenous Adomet. Tumor necrosis factor-
(TNF-) is
also a mediator of these models of hepatotoxicity. We investigated the
role of Adomet in lipopolysaccharide (LPS)-induced liver injury in rats
made deficient in both Adomet and choline. Rats were maintained on
either a methionine-restricted and choline-deficient (MCD) diet or a
diet containing sufficient amounts of all nutrients [methionine
and choline sufficient (MCS)] and then administered either LPS or
saline. MCS-LPS rats had normal liver histology and no change in serum
transaminases compared with the MCS-saline control group. MCD-saline
rats had hepatosteatosis but no necrosis, and a five- to sevenfold
increase in transaminases vs. the MCS-saline group. MCD-LPS rats
additionally had hepatonecrosis and a 30- to 50-fold increase in
transaminases. Exogenous Adomet administration to MCD-LPS rats
corrected the hepatic deficiency of Adomet but not of choline,
prevented necrosis but not steatosis, and attenuated transaminases.
Serum TNF- was sixfold higher in MCD rats even without LPS challenge
and 300-fold higher with LPS challenge. Exogenous Adomet attenuated
increased serum TNF- in MCD-LPS rats.
tumor necrosis factor-; choline deficiency; liver injury
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