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production in rats given enteral ethanol
1 Laboratory of Hepatobiology and Toxicology, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill 27599-7365; and 2 Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709
This study determined whether free radical formation by
the liver, tumor necrosis factor (TNF)-
production by isolated
Kupffer cells, and plasma endotoxin are affected by dietary saturated fat. Rats were fed enteral ethanol and corn oil (E-CO) or
medium-chain triglycerides (E-MCT) and control rats received corn oil
(C-CO) or medium-chain triglycerides (C-MCT) for 2 wk. E-CO rats
developed moderate fatty infiltration and slight inflammation; however, E-MCT prevented liver injury. Serum aspartate aminotransferase levels,
gut permeability, and plasma endotoxin doubled with E-CO but were
blunted ~50% with E-MCT. In Kupffer cells from E-CO rats, intracellular calcium was elevated by lipopolysaccharide (LPS) in a
dose-dependent manner. In cells from E-MCT rats, increases were blunted
by ~40-50% at all concentrations of LPS. The LPS-induced increase in TNF- production by Kupffer cells was dose dependent and
was blunted by 40% by MCT. E-CO increased radical adducts and was
reduced ~50% by MCT. MCT prevent early alcohol-induced liver injury,
in part, by inhibition of free radical formation and TNF- production
by inhibition of endotoxin-mediated activation of Kupffer cells.
tumor necrosis factor-; intracellular calcium; free radicals; alcohol
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