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Am J Physiol Gastrointest Liver Physiol 275: G125-G129, 1998;
0193-1857/98 $5.00
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Vol. 275, Issue 1, G125-G129, July 1998

S-adenosylmethionine deficiency and TNF-alpha in lipopolysaccharide-induced hepatic injury

Rajender K. Chawla1,2, Walter H. Watson1,2, Charles E. Eastin1,2, Eun Y. Lee3, Jack Schmidt1,2, and Craig J. McClain1,2

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-alpha (TNF-alpha ) 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-alpha was sixfold higher in MCD rats even without LPS challenge and 300-fold higher with LPS challenge. Exogenous Adomet attenuated increased serum TNF-alpha in MCD-LPS rats.

tumor necrosis factor-alpha ; choline deficiency; liver injury


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